Macular Degeneration Research

Macular Degeneration Therapeutics Market is Forecast to Show High Growth Rate, Doubling in Size by 2017

2011-01-29T07:38:00.000-08:00

Macular Degeneration - Pipeline Assessment and Market Forecasts to 2017 is an essential source of information and analysis on the global Macular Degeneration market. The report identifies the key trends shaping and driving the global Macular Degeneration market. The report also provides insights on the prevalent competitive landscape and the emerging players expected to significantly alter the market positioning of the current market leaders. Most importantly, the report provides valuable insights on the pipeline products within the global Macular Degeneration sector. This report is built using data and information sourced from proprietary databases, primary and secondary research and in-house analysis by a team of industry experts.

The authors valued the global macular degeneration therapeutics market at $1.3 billion in 2009. It is expected to grow to $3.0 billion with a Compound Annual Growth Rate (CAGR) of 10.4% by 2017. This growth is primarily attributed to the increase in the aged population across the world. Macular degeneration is a common disease that affects people above 50 years of age. Incidence is high in patients who are above 70 years. The growth will be supported by increased competition between the traditionally used off label products and the newly approved drugs and is expected to continue in the future. In 2009, Lucentis (ranibizumab), a blockbuster drug from Genentech, was the leading player in the global macular degeneration therapeutics market. Avastin is one of Genentech's blockbuster drugs, approved for various types of cancer. Avastin was widely used as an off-label drug by patients with macular degeneration before the approval of Lucentis.

Competition in the Macular Degeneration Therapeutics Market is Expected to Intensify The leading companies in the global macular degeneration therapeutics market are Genentech, Osi Eyetech Inc. and QLT Ltd. Together, these companies accounted for more than 95% of the global macular degeneration therapeutics market in 2009.

Genentech, with its blockbuster drug Lucentis, was the market leader with a share of more than 90%, followed by Visudyne (verteporfin). However, companies such as Novartis AG, Bayer/Regeneron Pharma, Adeona Pharma, Ophthotech Corp, Alcon Inc, Pfizer Inc, Acucela Inc, Alimera Sciences, Neurotech Pharma and Allergan Inc have the most technologically advanced products in their pipeline portfolios and are expected to attract most of the investors attention. The global macular degeneration therapeutics market has seen some intense competition in recent times, which is expected to further intensify over the coming years.

GlobalData, the industry analysis specialist, has released its new report, Macular Degeneration - Pipeline Assessment and Market Forecasts to 2017. The report is an essential source of information and analysis on the global Macular Degeneration market. The report identifies the key trends shaping and driving the global Macular Degeneration market. The report also provides insights on the prevalent competitive landscape and the emerging players expected to significantly alter the market positioning of the current market leaders. Most importantly, the report provides valuable insights on the pipeline products within the global Macular Degeneration sector. This report is built using data and information sourced from proprietary databases, primary and secondary research and in-house analysis by Our team of industry experts.

GlobalData valued the global macular degeneration therapeutics market at $1.3 billion in 2009. It is expected to grow to $3.0 billion with a Compound Annual Growth Rate (CAGR) of 10.4% by 2017. This growth is primarily attributed to the increase in the aged population across the world. Macular degeneration is a common disease that affects people above 50 years of age. Incidence is high in patients who are above 70 years. The growth will be supported by increased competition between the traditionally used off label products and the newly approved drugs and is expected to continue in the future. In 2009, Lucentis (ranibizumab), a blockbuster drug from Genentech, was the leading player in the global macular degeneration therapeutics market. Avastin is one of Genentechs blockbuster drugs, approved for various types of cancer. Avastin was widely used as an off-label drug by patients with macular degeneration before the approval of Lucentis.

Scope The report provides information on the key drivers and challenges of the Macular Degeneration market. Its scope includes: Annualized global Macular Degeneration market revenues data from 2001 to 2009, forecast for eight years to 2017. Pipeline analysis data providing a split across the different phases, mechanisms of action being developed and emerging trends. Pipeline candidates fall under major therapeutic classes such as VEGF inhibitors, angiogenesis inhibitors, C5a receptor antagonists, antioxidants, tyrosine kinase inhibitosr, clotting factor inhibitors, cyclooxygenase inhibitors, RPE inhibitors, antioxidants, PDGF inhibitors, chemokine inhibitors, IL-2 inhibitors, retinol protein binders, a51 integrin antagonist, protein C3 inhibitors and mRNA targeting agents. Analysis of the current and future competition in the global Macular Degeneration market. Key market players covered are Novartis AG, Bayer Pharma, Adeona Pharma, Ophthotech Corp., Alcon Inc, Pfizer Inc, Acucela Inc, Alimera Sciences, Neurotech Pharma, and Allergan Inc. Insightful review of the key industry drivers, restraints and challenges.

Each trend is independently researched to provide a qualitative analysis of its implications. Key topics covered include strategic competitor assessment, market characterization, unmet needs and the implications for the Macular Degeneration therapeutics market.

Reasons to buy The report will enhance your decision making capability. It will allow you to: Develop and design your in-licensing and out-licensing strategies through a review of pipeline products and technologies and by identifying the companies with the most robust pipeline. Develop business strategies by understanding the trends shaping and driving the global Macular Degeneration market. Drive revenues by understanding the key trends, innovative products and technologies, market segments and companies likely to impact the global Macular Degeneration market in future. Formulate effective sales and marketing strategies by understanding the competitive landscape and by analyzing the performance of various competitors. Identify emerging players with potentially strong product portfolios and create effective counter-strategies to gain a competitive advantage. Organize your sales and marketing efforts by identifying the market categories and segments that present maximum opportunities for consolidations, investments and strategic partnerships. What's the next big thing in the global Macular Degeneration market landscape? Identify, understand and capitalize.

Key Topics Covered: 1 Summary 2 Macular Degeneration Therapeutics: Disease Overview 3 Macular Degeneration Therapeutics: Market Characterization 4 Macular Degeneration Therapeutics: Competitive Assessment 5 Macular Degeneration Therapeutics: Pipeline Assessment 6 Global Macular Degeneration Therapeutics: Implications for Future Market Competition 7 Macular Degeneration Therapeutics: Future Players in the Macular Degeneration Disease Market 8 Macular Degeneration Therapeutics: Appendix Companies Mentioned: Alcon Inc. Novartis AG Ophthotech Corporation Pfizer Inc Acucela Inc. Regeneron Pharmaceuticals, Inc.

Age-related macular degeneration is growing with the graying American population

2011-01-23T11:01:00.000-08:00

By LESLIE BARKER GARCIA

DALLAS — Jennifer Tyler was driving down a country road in Oklahoma a couple of years ago when she noticed something odd. The telephone poles all had kinks in them.
"I thought, 'Wow, what's all that about?'" says Tyler, a Dallas fundraising consultant. "They all had distinctive bends in the middle."She pulled off the road and called a friend. "I knew something bad was happening," she says. "It was nothing I could ignore."Her friend referred Tyler to Texas Retina Associates. Tyler made an appointment and was diagnosed as having age-related macular degeneration.

AMD is a disease that causes significant vision loss in 1.75 million Americans. More than 10 million suffer from various forms of this potentially sight-stealing disease, more than glaucoma and cataracts combined, according to the American Macular Degeneration Foundation.By 2020, as the population ages, that number is expected to double.In addition, says Dr. Karl Csaky (pronounced like chalky) of the Retina Foundation of the Southwest, "more severe forms will be more of an issue."
"People who are in their 70s and 80s are extremely active," says Csaky, head of the foundation's Harrington Molecular Laboratory and an ophthalmologist with Texas Retina Associates. "If you had even a relatively small disturbance in vision, that could be extremely devastating in terms of what you're used to doing."Some vision disturbances, such as difficulty reading small print, are inherent with aging. The lenses of our eyes change and can no longer focus close up, so we rely on reading glasses.

Macular degeneration goes beyond the normal aging process. It affects the center of the retina; specifically, the 0.1 percent that's responsible for 99.9 percent of our fine vision, Csaky says."Unfortunately," Csaky says, "the central part is what gives you quality of life, the ability to read, drive, play golf, to discern faces."
He uses the analogy of a camera to explain the difference between normal eye aging and macular degeneration."The lens of the eye is like the lens of a camera," he says. "Cataracts are when the lens of the camera gets cloudy and the picture gets fuzzy. The solution? Change your lens, which is what cataract surgery is."In macular degeneration, your film has gotten old. We can change lenses, put in a special lens, and still have a bad picture because the film is starting to decay."

Macular degeneration has no cure, but those involved in studying and treating it point out glimmers of hope:Though it may cause legal blindness, rendering some victims unable to drive or read, it won't cause total blindness.Most kinds never progress past the initial stage. Diagnosis is not "a death sentence for vision," Csaky says.

Treatments can slow down and sometimes reverse the more severe cases of the condition. Diagnostic tools can catch it in its early stages.To check for it, "We dilate your eyes, use a lens and look for yellow spots (drusen) or pigmentation changes or bleeding," says Dr. Yuguang He, associate professor of ophthalmology at the University of Texas Southwestern Medical Center and a specialist in age-related macular degeneration. "It's not like it takes a blood test or X-ray to diagnose. We just look at it."

The sooner it's found, the better, he says. "There is a window in which we can do treatments."Most treatments are geared toward the more advanced form called wet macular degeneration. The early stage is called dry, which can progress to late-severe dry and sometimes lead to wet.Progression from the dry form to wet can be rapid. Tyler went to a doctor when she first had symptoms, so he was able to diagnose the disease early. Thus, she's been able to receive a relatively new and often successful treatment: a monthly shot directly into each of her eyes."It's psychologically and emotionally very draining," says Tyler, whose father has the dry variety of the disease.

The shot, explains Csaky, her doctor, inhibits a protein responsible for blood vessels growing and bleeding under the retina."We're not curing the disease," he says. "We're inhibiting, with a drug, a protein that's constantly being made, and with the injection it disappears for four to six weeks. The blood vessels are still there in a dormant state. If you don't treat them, they start to grow back."It's not comfortable, but patients tolerate it well, he says, though occasionally "we have a loved one faint who's watching. We use a topical anesthetic and a very, very small needle."

Although there is no surefire way to prevent the disease, studies have shown that eating fish two or more times per week helps reduce the risk, he says. "I take fish oil. I'm 54 years old and take it not only to prevent AMD but also to protect my heart, help my cholesterol. I tell patients, something good for your heart has to be good for your eyes."He also points out the Age-Related Eye Disease study of the National Eye Institution. Participants took large quantities of vitamins A and C, as well as zinc, copper and beta carotene. The regimen neither prevents the disease nor, in the study, did it have any effect on the dry form, but it "slowed the progression of the wet variety by 20 percent," he says.

Tyler, who declined to give her age, manages her ailment as best she can, getting injections and participating in a study. She is constantly aware of her surroundings, on the lookout for any line in a grid that appears curvy or wavy. She checks the spindles on her staircase, "whatever's around me," for possible distortion."It was never even in my mind, as driven and focused as I am in my career, that I wouldn't be responsive to it," she says. "It's your vision for heaven's sake. How scary is that?

"You can work with it and make it a positive thing, or it can devastate you. You make these choices in life. What am I going to do about it? Is it going to define me, or am I going to help define it?"Age-related macular degeneration (AMD) is the No. 1 cause of irreversible vision loss among senior citizens, according to the Retina Foundation of the Southwest. Some risk factors:

Caucasians are more likely to contract AMD than other races."If you're a Caucasian older than 65, there's a 20 percent chance you'll get it," says Dr. Yuguang He, associate professor of ophthalmology at UT Southwestern Medical Center. "If you're Chinese or Japanese, less than 5 percent. African-Americans have it much less than Caucasians."Yet, "as the Japanese adopted our diet, their incidence has gone up," says Dr. Karl Csaky of the Retina Foundation of the Southwest and Texas Retina Associates.

Smoking increases incidence."Cigarette smokers are 20 times more likely to develop AMD than nonsmokers," he says. "The chances are very, very high."

If one eye is affected, the other eye will be, too.It's important to periodically cover up the eye that has it to see whether the other eye is seeing distortions, too.Genetics play a factor."If your parents have it, there's an increased risk you'll get it, but it's not a guarantee," he says. "We're still struggling with the practical implications of these genetic associations other than scaring people."

Aarkstore Enterprise Macular Degeneration, Pipeline Review

2011-01-15T01:23:00.000-08:00

by: Pipeline Review,Q4

Aarkstore announce a new report “Macular Degeneration – Pipeline Review, Q4 2010 ” through its vast collection of market research report.

“Macular Degeneration Pipeline Review, Q4 2010”, provides an overview of the Macular Degeneration therapeutic pipeline. This report provides information on the therapeutic development for Macular Degeneration, complete with latest updates, and special features on late-stage and discontinued projects. It also reviews key players involved in the therapeutic development for Macular Degeneration. “Macular Degeneration-Pipeline Review 2010, Q4 2010” is built using data and information sourced from proprietary databases, Company/University websites, SEC filings, investor presentations and featured press releases from company/university sites and industry-specific third party sources, put together.

Scope

- A snapshot of the global therapeutic scenario for Macular Degeneration.
- A review of the Macular Degeneration products under development by companies and universities/research institutes based on information derived from company and industry-specific sources.
- Coverage of products based on various stages of development ranging from discovery till registration stages.
- A feature on pipeline projects on the basis of monotherapy and combined therapeutics.
- Coverage of the Macular Degeneration pipeline on the basis of therapeutic class, route of administration and molecule type.
- Profiles of late-stage pipeline products featuring sections on product description, mechanism of action and research & development progress.
- Key discontinued pipeline projects.
- Latest news and deals relating to the products.

- Identify and understand important and diverse types of therapeutics under development for Macular Degeneration.
- Identify emerging players with potentially strong product portfolio and design effective counter-strategies to gain competitive advantage.
- Plan mergers and acquisitions effectively by identifying players with the most promising pipeline.
- Devise corrective measures for pipeline projects by understanding Macular Degeneration pipeline depth and focus of Macular Degeneration therapeutics.
- Develop and design in-licensing and out-licensing strategies by identifying prospective partners with the most attractive projects to enhance and expand business potential and scope.
- Modify the therapeutic portfolio by identifying discontinued projects and understanding the factors that drove them from pipeline., provides an overview of the Macular Degeneration therapeutic pipeline. This report provides information on the therapeutic development for Macular Degeneration, complete with latest updates, and special features on late-stage and discontinued projects. It also reviews key players involved in the therapeutic development for Macular Degeneration. “Macular Degeneration-Pipeline Review 2010, Q4 2010” is built using data and information sourced from proprietary databases, Company/University websites, SEC filings, investor presentations and featured press releases from company/university sites and industry-specific third party sources, put together.

FDA Approves Company's Clinical Trial Of hESCs- based Treatment for AMD

2011-01-09T01:24:00.000-08:00

by: Advanced Cell Technology, Inc.

Advanced Cell Technology, Inc. (OTCBB: ACTC), a regenerative medicine company based in Marlborough, Mass., announced on January 3 that the U.S. Food and Drug Administration (FDA) has cleared its Investigational New Drug (IND) application to treat dry age-related macular degeneration (AMD) using retinal pigment epithelial (RPE) cells derived from human embryonic stem cells (hESCs).

ACT is now permitted to launch a Phase 1-2 multicenter clinical trial to treat patients with dry AMD, the most common form of macular degeneration in the world.

There are no treatments available for this prevalent disease of an aging global population. According to the company, dry AMD, representing a substantial global market opportunity and afflicts between 10-15 million Americans.

Age-Related Macular Degeneration has two predominant forms, wet and dry. Dry AMD is the most common form, accounting for almost 90 percent of all cases. The progress of dry AMD includes a breakdown or thinning of the layer of RPE cells in the patient’s macula, the region at the center of the retina responsible for high acuity vision. Over time, the progressive loss of RPE cells and accompanying loss of photoreceptors can cause severe vision loss and even blindness.

“ACT is now the first company to receive FDA clearance for two hESC trials, and is now a true translational leader in the field of regenerative medicine,” said interim CEO Gary Rabin. “It marks a major step forward, not just within the stem cell sector, but, potentially for modern healthcare techniques. We plan to proceed into the clinic with both of our hESC-based programs as quickly as possible.”

The Phase 1-2 trial will be a prospective, open-label study that is designed to determine the safety and tolerability of the RPE cells following sub-retinal transplantation into patients with dry AMD. Twelve patients will be enrolled in the study at multiple clinical sites. Sites currently under consideration are the Jules Stein Eye Institute at UCLA, and the Ophthalmology Department at Stanford University School of Medicine. Additional sites may be considered.

“Dry AMD is the leading cause of blindness in individuals over the age of 55,” said Robert Lanza, M.D., chief scientific officer. “As the population ages, the incidence of AMD is expected to double over the next 20 years, further exacerbating this unmet medical need. Using our clinical-grade hESC lines, we are able to generate a virtually unlimited and reproducible supply of healthy RPE cells. Because only a small number of cells (50-200K) are needed to treat each patient, manufacturing and distribution of the therapeutic product is scalable with many similarities to the drug businesses that pharmaceutical companies understand well. Based on our animal model studies, we are very excited about the opportunity to treat patients. In a rat model of macular degeneration, we have seen a remarkable improvement in visual performance over untreated animals, without any adverse effects. We have also maintained near-normal function in a mouse model of Stargardt’s Disease, a form of juvenile macular degeneration. In addition to this trial, we plan to concurrently use our RPE cells in our Phase I/II Clinical Trial for Stargardt’s Disease, which received the green light from the FDA in November. We hope to see a similar benefit in both Stargardt’s Disease and Dry AMD patients.”

ACT’s dry AMD therapeutic program uses RPE cells derived from hESCs to replace the lost RPE cells in the patient’s eyes. ACT’s proprietary RPE cell manufacturing process is protected by a number of broad patents, as is the use of hESC-derived RPE cells for treating macular degeneration. While the initial portion of the clinical trial will focus on safety, in subsequent clinical trials the company hopes to demonstrate that the RPE cells injected into the retinal space will be capable of slowing or halting progression of the disease, and potentially even restoring some visual acuity to patients.

“It is estimated that over ten million Europeans suffer from age-related macular degeneration, representing a vast unmet need and a significant market opportunity,” commented Edmund Mickunas, vice president of regulatory affairs. “We are moving ahead aggressively to seek regulatory clearance from the European Medicines Agency to conduct clinical trials in Europe.”

Case Western Reserve receives $10 million to study Retina Disease

2011-01-02T16:29:00.000-08:00

by: Jessica Studeny

The Departments of Pharmacology and Ophthalmology and Visual Sciences at Case Western Reserve University School of Medicine have been awarded a $10.1 million grant from the National Eye Institute (NEI) to research and develop new treatments for diseases of the retina, a leading cause of blindness.

"The grant strongly positions the School of Medicine and collaborating organizations to play a significant role in advancing the treatment of retinal diseases in order to restore quality of life to countless patients," said Jonathan H. Lass, MD, professor and chair of the Department of Ophthalmology and Visual Sciences at Case Western Reserve School of Medicine and director of the University Hospitals Eye Institute. "It is the largest grant of its kind ever awarded to the university by the National Eye Institute, a tremendous achievement."

The NEI, part of the National Institutes of Health (NIH), will award the grant over five years, funding the work of researchers in the Departments of Pharmacology, Ophthalmology, and Biomedical Engineering at the School of Medicine who are working in collaboration with the Retinal Therapeutics Study Group. This interdisciplinary consortium of investigators is screening FDA-approved drugs for their potential application to the treatment of eye diseases affecting the retina.

The combined group, which also includes researchers from the Cincinnati Drug Discovery Center, the University of Pennsylvania and Washington University, aims to accelerate the rate at which basic science discoveries are used to develop new therapies for complex retinal disorders and diseases.

Conditions affecting the retina, the tissue in back of the eye responsible for vision, are a primary cause of blindness in adults in the United States. Such diseases include age-related macular degeneration (AMD), the main cause of blindness in adults over the age of 55. More than 1.3 million people in the U.S. are legally blind and 8 to 10 million aging individuals show signs of developing AMD, an incurable eye disease characterized by damage to the retina and the loss of central daylight vision.

"The research being funded by the NIH is critical to availing patients of new, more effective treatments, particularly for diseases like AMD, for which there is currently no cure," says Krzysztof Palczewski, PhD, John H. Hord Professor, chair of the Department of Pharmacology, and principal investigator and director of the research funded by the new NEI grant. "Our goal is to develop new drugs based on the screening of FDA-approved drugs to evaluate their effectiveness in treating retinal diseases."

Researchers will employ a range of scientific expertise and state-of-the-art physiological, chemical and analytical imaging technologies to test potential retinal disease therapies in basic research models. A non-invasive imaging technology developed at Case Western Reserve by Dr. Palczewski's research group will facilitate monitoring of the retina to detect molecular changes, defects, or harmful toxins in the retina.

FDA-approved drugs will be screened for their potential application in research models engineered to mimic conditions such as AMD, Stargardt's disease (a form of inherited juvenile macular degeneration) and retinitis pigmentosa (a group of inherited retinal disorders characterized by progressive peripheral vision loss). The drug-screening process is designed to accelerate the process of drug development before clinical testing in humans.

Dr. Palczewski is working with researcher Akiko Maeda, MD, PhD, senior instructor in the Departments of Ophthalmology and Pharmacology; and Zheng-Rong Lu, PhD, professor of biomedical engineering; to hone in on existing drugs with chemical properties and initial research results that suggest they may provide a basis for developing new drugs for treating retinal diseases like AMD.

The research builds upon previous work in Dr. Palczewski's laboratory which identified mechanisms in the eye responsible for metabolizing vitamin A, an essential step in triggering the nerve signals sent to the brain to enable vision. Researchers determined that in healthy patients, this visual cycle operates rapidly. However, in older patients and those with AMD and Stargardt-like diseases, one of the critical biochemical reactions in the series that recycle vitamin A is slowed. This allows a toxic byproduct produced by the breakdown of vitamin A to accumulate, which damages the retina over time, probably contributing to the development of AMD and/or impairing vision.

The combined teams in Ophthalmology and Pharmacology are now looking for drugs that can target the mechanism that captures toxic vitamin A metabolites, to neutralize and counter the build-up of any visual cycle toxic byproduct, as a means of preventing or controlling retinal diseases. "Current treatments for AMD focus on management of the late stages of the disease. These studies could result in treatments at the earlier stages and save more vision as a result" says Dr. Lass.

In addition to testing existing FDA-approved drugs for their ability to reduce toxic substances within the retina, priorities for the NIH-funded research also include evaluating existing FDA-approved drugs as potential lead compounds for retinal diseases because these drugs have already been proven safe and effective in basic research and clinical studies for other indications. Researchers will likewise assess the ability of potential compounds to penetrate and remain in the eye without negatively affecting vision and they will explore and develop new drug delivery systems to achieve and maintain therapeutic drug concentrations in the eye.

"We have an idea as to what drugs could be most effective for our purposes," said Dr. Maeda, who relocated from Japan to the United States to work with Dr. Palczewski. She is the study's co-principal investigator and a group leader who is responsible for basic research models. "During my clinical practice in ophthalmology, I was very frustrated with the lack of treatment options for many patients with retinal degenerative diseases, and I became determined to dedicate myself to developing new treatments for these patients through basic science research. I am very excited to develop our ideas for treating currently incurable retinal diseases."

Dr. Palczewski and his team have already examined 24 FDA-approved drugs, from antibiotics to drugs fighting cancer and infectious diseases, for their ability to attack the buildup of harmful toxins in the retina. These studies were done with mice that were genetically engineered to mimic Stargardt's disease. At least 16 of the drugs tested have already demonstrated the potential to limit the progression of retinal diseases. The resulting data provided the basis for funding the $10 million NIH grant request.

About Case Western Reserve University School of Medicine

Founded in 1843, Case Western Reserve University School of Medicine is the largest medical research institution in Ohio and is among the nation's top medical schools for research funding from the National Institutes of Health. The School of Medicine is recognized throughout the international medical community for outstanding achievements in teaching. The School's innovative and pioneering Western Reserve2 curriculum interweaves four themes--research and scholarship, clinical mastery, leadership, and civic professionalism--to prepare students for the practice of evidence-based medicine in the rapidly changing health care environment of the 21st century. Nine Nobel Laureates have been affiliated with the school of medicine.

Annually, the School of Medicine trains more than 800 MD and MD/PhD students and ranks in the top 20 among U.S. research-oriented medical schools as designated by U.S. News & World Report "Guide to Graduate Education."

The School of Medicine's primary affiliate is University Hospitals Case Medical Center and is additionally affiliated with MetroHealth Medical Center, the Louis Stokes Cleveland Department of Veterans Affairs Medical Center, and the Cleveland Clinic, with which it established the Cleveland Clinic Lerner College of Medicine of Case Western Reserve University in 2002.

Age-Related Macular Degeneration Research from University of Bristol

2010-12-27T05:56:00.000-08:00

by: University
"Neovascular age-related macular degeneration (nvAMD) is a chronic, progressive disease of the central retina, and its prevalence is expected to rise with the aging population. Using a bottom-up approach based on retrospective data, this cross-sectional study estimated average annual direct costs of nvAMD to be A 4,047 pound, and average annual indirect costs to be A 449 pound," scientists in Bristol, the United Kingdom report.

"An attempt to measure intangible costs through willingness-to-pay yielded a lower response rate and estimated intangible costs to be 11.5% of monthly income. Direct costs were significantly higher for male participants, for those who have mild or moderate visual impairment in both eyes, and for those who have been diagnosed for a shorter time," wrote K.M. Ke and colleagues, University of Bristol.

The researchers concluded: "The findings of this study suggest that the availability of early diagnosis, effective treatment, support services, and sustained research into the management of nvAMD may reduce the burden of visual impairment caused by nvAMD to affected individuals and the state."

Ke and colleagues published their study in European Journal of Health Economics (The direct, indirect and intangible costs of visual impairment caused by neovascular age-related macular degeneration. European Journal of Health Economics, 2010;11(6):525-531).

For additional information, contact K.M. Ke, University of Bristol, Bristol Dental School, Dept. of Oral & Dental Science, Lower Maudlin St., Bristol BS1 2LY, Avon, UK.

The publisher's contact information for the European Journal of Health Economics is: Springer, 233 Spring St., New York, NY 10013, USA.

Keywords: City:Bristol, Country:United Kingdom, Age-Related Macular Degeneration, Retinal Degeneration, Retinal Diseases

Genetic Testing for AMD is here Today

2010-12-20T05:39:00.000-08:00

by:Diana Shechtman OD FAAO & Steven Ferrucci OD FAAO

Age-Related macular degeneration (AMD) is a progressive disease and the leading cause of vision loss among the elderly, affecting central vision required for daily activities such as driving and reading. There are a number of factors affecting AMD, such as advanced age, smoking, UV exposure, overall health (that contribute to high blood pressure, obesity, diet) and family history. Many factors may be modified and yet others like genetics cannot. Although AMD may seem to be hereditary in some families and not others, genetics have been shown to contribute significantly to the disease. Multiple twin and sibling studies have collaborated to the familial nature of the disease. First-degree relatives of patients with AMD are at a significantly increased risk for the disease. Furthermore, large epidemiological studies have suggested a strong genetic risk factor for AMD. In fact, the risk of developing AMD increases 4 fold among patients with a positive family history. In 2005 a breakthrough occurred in the area of genetic research and AMD; Klein and associates discovered a strong link between AMD and certain genetic variants. Similarly, numerous other genes have been implicated in AMD, which may increase the risk of AMD up to 70%.
Until recently there was no test to help determined patient’s inherited risk for AMD. Today, Macula Risk (ArcticDX, Toronto, Ontario) is a genetic test specifically designed to determine genetic predisposition to AMD and vision loss attributed to the more advanced stage of the disease.
Macula Risk  genetic test separates individuals into one of 5 macula risk (MR) categories, with MR 3 through 5 representing an increased risk for the more advance stage of the disease. This accounts for approximately 20% of the general population. MR1 has less than a 5% risk of the advanced stage of the disease, while MR 5 carries greater than 55% risk. These results can aid the doctor in devising a specific management plan and follow-up protocol in order to reassure early intervention to prevent vision loss.
The test only requires a simple in-office cheek swab, which is sent directly to the genetic lab. The report includes test results and written genetic support information (including access to genetic counseling). Macula Risk genetic testing is covered by most insurance providers, including Medicare, as long as the specific diagnosis (ICD-9) are identified by the doctor. The prognostic genetic test is intended for patients who have a diagnosis of early or intermediate AMD. Thus, the “at risk patient,” would have to pay a fee for the test.
Despite our best efforts and new treatment options available today, many people are still losing vision from AMD. New advancements in the area of AMD are becoming an integral part in preventing future visual deterioration. AMD is affected by both environmental and genetic factors that interact with one another to determine prevalence and progression of the disease. Furthermore, at this time we do not know all of the genes linked to AMD. Hence, genetic testing in the area of AMD is only a risk indicator and cannot predict “without a shadow of a doubt,” which patients will and which will not develop the disease. However, this test provides a genetic profile screening to help identify those at risk as well as aids in tailoring a distinct management approach for those with the disease. With various researches devoted to treatment options for AMD, genetic testing in the area of AMD is at the frontier of providing crucial information.
REFERENCES
1. Swaroop, Branham KE, Chen W, Abecasis G. Genetic susceptibility to age-related macular degeneration: a paradigm for dissecting complex disease traits. Hum Mol Genet 2007; 16: 174-82.
2. Klein ML, Mauldin WM, Stoumbos VD. Heredity and age-related macular degeneration. Observations in monozygotic twins. Arch Ophthalmol. 1994; 112: 932-7.
3. Meyers SM, Greene T, Gutman FA. A twin study of age-related macular degeneration. Am J Ophthalmol. 1995; 120: 757-66.
4. Heiba IM, Elston RC, Klein BE, et al. Sibling correlations and segregation analysis of age-related maculopathy: The Beaver Dam Eye Study. Genet Epidemiol. 1994; 11: 51-67.
5. Klaver CC, Wolfs RC, Assink JJ, et al. Genetic risk of age-related maculopathy. Population-based familial aggregation study. Arch Ophthalmol. 1998; 116: 1646-51.
6. Seddon JM, Ajani UA, Mitchell BD. Familial aggregation of age-related maculopathy. Am J Ophthalmol. 1997; 123: 199-206.
7. Klein RJ, Zeiss C, Chew EY, et al. Complement Factor H Polymorphism in Age-Related Macular Degeneration. Science 2005; 308: 385-389.
8. Seddon JM, Reynolds R, Maller J, Fagerness JA, Daly MJ, Rosner B. Prediction model for prevalence and incidence of advanced age-related macular degeneration based on genetic, demographic, and environmental variables. Invest Ophthalmol Vis Sci 2009; 50 (65): 2044-53.
9. www.macularisk.com/en/physicians/order.html (accessed Dec. 14th , 2010)

The link Between Age-Related Macular Degeneration and Cardiovascular Disease

2010-12-11T07:30:00.000-08:00

by:Johns Hopkins Health Alert

Several studies have found that people with age-related macular degeneration (AMD) are more likely to have heart disease than those without age-related macular degeneration. A U.S. Medicare study, for example, found that elderly people with age-related macular degeneration were 20% more likely to have a heart attack than their counterparts who didn't have age-related macular degeneration. And a large Australian study, reported in the British Journal of Ophthalmology, suggests that age-related macular degeneration increases the risk of dying from coronary heart disease or stroke.

The researchers used data from nearly 3,000 participants, age 49 and older, in the Blue Mountains Eye Study -- none with a history of coronary heart disease or stroke at enrollment. They found that people younger than age 75 who had early signs of age-related macular degeneration at the study's start were twice as likely to die of coronary heart disease as their counterparts who did not have early signs. However, there was no increased risk of dying of a stroke in this group.

People with late age-related macular degeneration at the beginning of the study who were under age 75 had five times the risk of dying of coronary heart disease and 10 times the risk of dying of a stroke. The link between late age-related macular degeneration and risk of death from cardiovascular disease should be interpreted cautiously, warn the researchers, because there were so few people with late age-related macular degeneration at study entry.

Surprisingly, the researchers found no increased risk of death from cardiovascular disease among people over age 75 with age-related macular degeneration. They speculate that past 75, patients died of other serious health conditions that overshadowed the connection.

Take-away message: What's behind the link between age-related macular degeneration and cardiovascular disease? Some researchers suspect that age-related macular degeneration and cardiovascular diseases may share a common genesis: for instance, atherosclerosis, inflammation, and oxidative stress (the cell damage caused by free radicals) are known to affect both conditions. Another alternative: age-related macular degeneration may simply be a disease of aging.

Medical Disclaimer: This information is not intended to be substituted for the advice of a physician. Johns Hopkins Health Alerts

SiemCells, Inc. Expands SC Proven(R) Product Portfolio With launch of Proprietary Human Cell Detection Antibodies

2010-12-07T02:52:00.000-08:00

Posted by: StemCells,Inc.

StemCells, Inc. (Nasdaq: STEM | PowerRating) announced today the launch of STEM101(TM), STEM121(TM) and STEM123(TM), three new antibody reagents that significantly improve the visualization of human cells, including human stem cells and their progeny. These high potency antibodies are the latest additions to the Company's growing SC Proven(R) portfolio of research products, and provide powerful, cost-effective tools for the detection, tracking and characterization of human cells both in vitro and when transplanted into animal models of human diseases.

"The commercial launch of these proprietary antibodies demonstrates our ongoing commitment to broaden our portfolio of innovative research products and to take advantage of the growing market for research-grade cells, media and reagents," said Stewart Craig, Senior Vice President, Development and Operations at StemCells, Inc. "Their utility has been proven by our scientists and by independent academic collaborators in the conduct of their research and development activities. These antibodies have also become the cornerstone of our extensive preclinical studies, which have allowed us to successfully advance our stem cell therapeutic candidates into multiple clinical trials. There is considerable demand for these reagents, so we are pleased to now make them available to the scientific community at large."

STEM101, STEM121 and STEM123 are human-specific mouse monoclonal antibodies that have been extensively used to detect the engraftment, migration and differentiation of human neural stem cells and human liver engrafting cells (hLEC(TM)) transplanted into rodents.1,2,3,4,5 These antibodies can be used for immunohistochemistry and immunofluorescence applications such as:

-- Quantifying the location and number of engrafted cells

-- Tracking the migration pattern of engrafted cells

-- Determining the nature of engrafted cells

-- Identifying specific differentiated human-derived cells such as

astrocytes
STEM101 recognizes the Ku80 protein found in human nuclei, STEM121 recognizes a cytoplasmic protein of human cells, and STEM123 recognizes human glial fibrillary acidic protein (GFAP).

About SC Proven Products

The SC Proven product portfolio comprises a range of specialty cell culture products that enable the standardized and reproducible production and propagation of highly purified stem cells and their differentiated progeny, as well as reagents for cell detection, isolation and characterization.

References

-- Kelly S, et al. Transplanted human fetal neural stem cells survive,

migrate, and differentiate in ischemic rat cerebral cortex. PNAS (2004)

101:11839-11844

-- Cummings B.J., et al. Human neural stem cells differentiate and promote

locomotor recovery in spinal cord-injured mice. PNAS (2005) 102:

14069-14074

-- Tamaki S.J., et al., Neuroprotection of Host Cells by Human Central

Nervous System Stem Cells in a Mouse Model of Infantile Neuronal Ceroid

Lipofuscinosis. Cell Stem Cell (2009) 5:310-319

-- Kallur T., et al. Human Fetal Cortical and Striatal Neural Stem Cells

Generate Region-Specific Neurons In Vitro and Differentiate Extensively

to Neurons After Intrastriatal Transplantation in Neonatal Rats. J

Neurosci Res. (2006) 84:1630-1644

-- Salazar D.L., et al., Human Neural Stem Cells Differentiate and Promote

Locomotor Recovery in an Early Chronic Spinal Cord Injury NOD-scid Mouse

Model. PLoS ONE (2010) 5: e12272

About StemCells, Inc.

StemCells, Inc. is engaged in the research, development, and commercialization of cell-based therapeutics and tools for use in stem cell-based research and drug discovery. In its therapeutic product development programs, StemCells is targeting disorders of the central nervous system and the liver. StemCells' lead product candidate, HuCNS-SC(R) cells (purified human neural stem cells), is currently in clinical development for the treatment of two fatal neurodegenerative disorders in children, and in preclinical development for spinal cord injury and retinal disorders such as age-related macular degeneration. StemCells also markets research products, including media and reagents, under the SC Proven(R)brand, and is developing stem cell-based assay platforms for use in pharmaceutical research, drug discovery and drug development. Further information about StemCells is available at www.stemcellsinc.com.

The StemCells, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=7014

Apart from statements of historical fact, the text of this press release constitutes forward-looking statements within the meaning of the U.S. securities laws, and is subject to the safe harbors created therein. These statements include, but are not limited to, statements regarding the ability of STEM101, STEM121 and STEM123 to enable and improve the visualization, detection, tracking and characterization of human cells both in vitro and when transplanted into animal models of human diseases; the clinical development of the Company's HuCNS-SC cells; the prospects for the Company to pursue non-therapeutic applications of its cell-based technologies; and the future business operations of the Company. These forward-looking statements speak only as of the date of this news release. The Company does not undertake to update any of these forward-looking statements to reflect events or circumstances that occur after the date hereof. Such statements reflect management's current views and are based on certain assumptions that may or may not ultimately prove valid. The Company's actual results may vary materially from those contemplated in such forward-looking statements due to risks and uncertainties to which the Company is subject, including those described under the heading "Risk Factors" in the Company's Annual Report
on Form 10-K for the year ended December 31, 2009, and in its subsequent reports on Form 10-Q and Form 8-K.

DeGette Hails Approval of Second Embryonic Stem Cell Human Trial

2010-11-28T09:36:00.000-08:00

by:PoliticalNews

Congresswoman Diana DeGette (CO-01) hailed the approval of the second human treatment trial using human embryonic stem cells. The test, just approved by the FDA, will be conducted by Advanced Cell Technology (ACT) and will focus on Stagart disease. Medical professionals believe a successful human trial will open the doors to the treatment of other, more common eye diseases such as macular degeneration. DeGette has been the leading Congressional advocate for federal funding of ethical embryonic stem cell research, as these investments drive breakthrough trials like the one announced this week.

“Embryonic stem cell research holds enormous promise for countless diseases,” said DeGette, “and the approval of this test is yet another step towards the breakthroughs it can bring for millions of Americans. I am excited to see the results of this, and other trials, and encourage my colleagues to recognize the enormous benefits of ethical embryonic stem cell research.”

Stagart’s disease affects central vision – e.g., reading and facial recognition – and can cause its victims to lose peripheral vision, only be able to see various levels of light, or ultimately go blind. This test will treat Stagart’s patients with healthy cells, created from embryonic stem cells, to replace the “scavenger cells” that deteriorate their vision.

The test is the second trial using embryonic stem cells to be approved in the United States. Last month, the Geron Corporation was permitted to conduct a trial involving embryonic stem cells to treat spinal cord injuries. Preliminary testing is still ongoing in that trial. Like the Geron trial, this latest trial will focus primarily on the safety and viability of embryonic stem cell use in the treatment of this condition. The Stagart’s trial will likely start early next year and 12 subjects will be treated.

“The approval of these two tests in such close order demonstrates how the investment by the federal government in ethical stem cell research is beginning to bear fruit for the millions of Americans facing debilitating diseases and conditions,” said DeGette. “The breakthroughs of these discoveries underscore the critical importance of finally codifying ethical stem cell research regulations, so our scientists and their critical work can no longer be subject to political whims.”

Chardan Capital Market Initiates Research Coverage of Stemcells

2010-11-22T10:38:00.000-08:00

by GlobeNewswire

PALO ALTO, Calif., - StemCells, Inc. /quotes/comstock/15*!stem/quotes/nls/stem (STEM 1.12, -0.02, -1.75%) announced today that Chardan Capital Markets (Chardan) initiated independent equity research coverage on the Company with a "Buy" recommendation and a 12-month price target of $1.45 per share. The new report, issued yesterday, was authored by Keay Nakae, Senior Analyst at Chardan.

Chardan is the second firm to initiate independent equity research coverage of StemCells, Inc. this year. Headquartered in New York, Chardan is an investment banking and institutional brokerage firm with a focus on micro, small, and mid-cap markets. More information about Chardan is available at www.chardancm.com. StemCells does not endorse or adopt the reports, projections or statements of any analyst.

About StemCells, Inc.

StemCells, Inc. is engaged in the research, development, and commercialization of cell-based therapeutics and tools for use in stem cell-based research and drug discovery. In its therapeutic product development programs, StemCells is targeting disorders of the central nervous system and the liver. StemCells' lead product candidate, HuCNS-SC(R) cells (purified human neural stem cells), is currently in clinical development for the treatment of two fatal neurodegenerative disorders in children, and in preclinical development for spinal cord injury and retinal disorders such as age-related macular degeneration. StemCells also markets stem cell research products, including media and reagents, under the SC Proven(R) brand, and is developing stem cell-based assay platforms for use in pharmaceutical research, drug discovery and drug development. Further information about StemCells is available at www.stemcellsinc.com.

UC Santa Barbara Part of International Research Collaboration Focusing on Age-Related Macular degeneration Cure

2010-11-15T19:37:00.000-08:00

By AScribe Newswire

SANTA BARBARA, Calif., Nov. 15 - An international collaboration between UC Santa Barbara, the Keck School of Medicine of the University of Southern California (USC), and several other research institutions, is bringing together leaders in the fields of stem cell biology, basic science, and ophthalmology to develop a treatment for blindness caused by age-related macular degeneration.

The California Project to Cure Blindness (CPCB) was formed with a $16 million California Institute for Regenerative Medicine (CIRM) "disease team" grant awarded in late 2009 to fund development of a stem cell-based treatment for age-related macular degeneration. As part of the CIRM Disease Team partnership program, an additional $4.1 million from Britain's Medical Research Council funds collaborative work at University College of London.

"UCSB scientists in the Center for Stem Cell Biology and Engineering and the Center for the Study of Macular Degeneration are excited to provide the basic research that will allow translation of stem cell research to the clinic," said Dennis Clegg, professor in UCSB's Department of Molecular, Cellular, and Developmental Biology, and co-director of the UCSB Center for Stem Cell Biology and Engineering. Both centers are part of UCSB's Neuroscience Research Institute. Grant funds totaling $2.5 million for this work were assigned to UCSB through USC.

The overall grant was awarded to principal investigator Mark Humayun, professor of ophthalmology, cell and neurobiology and biomedical engineering at the Keck School, and David R. Hinton, professor of pathology and ophthalmology at the Keck School. Co-investigator is Martin Pera, director of the Eli and Edythe Broad CIRM Center for Regenerative Medicine and Stem Cell Research at USC.

"With this collaboration, we hope to accelerate research on a stem cell-based therapy for age-related macular degeneration," said Humayun. "Age-related macular degeneration is the leading cause of irreversible vision loss, affecting one in three people age 75 or older. The CIRM grant enables us to work with numerous researchers and experts who are dedicated to finding the cure to this devastating medical condition."

The cause of blindness in age-related macular degeneration is the death of retinal pigment epithelial cells, which provide critical support of photoreceptor function and health. The project objective is to replace damaged retinal epithelium with healthy tissue derived from human embryonic stem cells to prevent loss of vision.

Stem cell therapy offers the possibility of a wider range of options for age-related macular degeneration patients, said Keck School Dean Carmen A. Puliafito. "While exciting new pharmaceuticals to treat age-related macular degeneration are now available, these are effective only in a select group of patients, and can be used only during a narrow time window," said Puliafito, an ophthalmologist whose academic focus is macular degeneration. "In contrast, stem cell therapy promises to be broadly applicable. The potential is tremendous."

CIRM President Alan Trounson noted that the disease team approach exemplified by the California Project to Cure Blindness could transform the direction of future research.

"Scientists have talked for years about the need to find ways to speed the pace of discovery," said Trounson. "CIRM, through the Disease Team Award Program, has encouraged applicants to form teams composed of the best researchers from around the world. The partnership between the California Project to Cure Blindness and Britain's Medical Research Council is a great example of CIRM's vision of a new standard for funding translational research."

Miracle Eye Implant Restores sight to Blind

2010-11-04T05:59:00.000-07:00

by Victoria Fletcher

A MAN who was totally blind can now read letters of the alphabet and the time on a clock face with a microchip implanted in his eye, it was revealed yesterday.

Experts said hopes of such a leap forward had previously existed “only in the realm of science fiction”.

But now researchers have shown it is possible to restore vision lost to disease with an electronic eye.

The study, by a team in Germany, will offer hope to the 25,000 Britons who are told they will go blind due to an inherited condition known as retinitis pigmentosa.

But it could also eventually treat the 300,000 who have macular degeneration which also leads to blindness.

The microchip, smaller than the tip of a pen and containing 1,500 tiny light sensors, fits into a natural space beneath the retina.

When an image comes through the lens of the eye it hits the sensors which send an electrical pulse to nerve cells at the back of the eye. These transmit the message to the brain.
Miikka can now tell an apple from a banana and right Professor Robert Maclaren

The device is powered by a thin cable that runs from the eye, out of the side of the skull and is attached to a battery behind the ear.

The new study reveals that three patients have been able to see grainy images of objects and recognise shapes after having the device fitted.

Finn Miikka Terho, 46, was able to walk around a room with ease, read his own name and even tell researchers they had spelt it wrongly.

He could recognise shades of grey, read the time from a clock and pick up an apple and a banana from the table in front of him.

Before the implant he was totally blind apart from being able to detect changes between light and dark.

The pilot study, published in the Proceedings of the Royal Society B Journal, means the technology behind the device works, is safe and is ready to be tested on a larger number of patients in a proper clinical trial.

Although it does not mean patients will ever be able to see normally, it does raise the prospect that the blind will be helped to see enough to regain some independence.

Prof Robert Maclaren, Professor of Ophthalmology at Oxford University, will conduct the next trial.

He said: “This is a big breakthrough, no two ways about it. To take someone who is blind and help them see again is pretty incredible.”

He added: “The successful testing of this electronic implant in Germany is without doubt a truly significant advance.

“One previously blind patient was able to read his own name with the implant switched on. Until now, this concept would have been considered only in the realms of science fiction.”

In recent years, scientists have helped to restore vision using a small camera mounted on spectacles.

This allowed a rough interpretation of an image beamed through a wire into the brain.

But the new device, developed by German scientist Prof Eberhart Zrenner, shows that the damaged light receptor cells in the eye can simply be replaced by a microchip.

The rest of the image is obtained by the natural eye. Prof Zrenner has now set up the technology firm Retinal Implant AG to develop the device.

Around one in 3,000 Britons have retinitis pigmentosa, which destroys light cells in the eye.The condition, triggered by a range of genes, is incurable and untreatable.
More than 10 times as many people have macular degeneration.

It usually affects older adults and leads to a loss of central vision, making it difficult or impossible to read or recognise faces although enough some peripheral vision remains.

Prof Maclaren said he was thrilled he could now tell patients with retinitis pigmentosa that there was hope ahead after years of having to tell them they would be left completely blind. And he said that although the device did not offer an amazing quality of vision, it would be significant for people who had previously been unable to see anything.

David Head, chief executive of the British Retinitis Pigmentosa Society, welcomed the news, calling it “a very significant advance”. But he said he wanted patients to realise that even this breakthrough would not restore their vision.
He added: “The technology is exciting and hopefully this will advance in the next few years but we have to temper it with reality.”

Up to 12 patients are expected to take part in the British study, due to start early next year at King’s College Hospital, London, and the Oxford Eye Hospital.It is hoped that when the device can be left in place for years instead of months, the brain may learn to interpret the grey and white images into far more accurate pictures of what the eye is really seeing.

OGI invests in personalized medicine for age-related macular degeneration

2010-11-02T05:22:00.000-07:00

by administrator

Established in 2007 and based in Toronto, ArcticDx has developed a test, Macula Risk®, the first of its kind and specifically designed to determine one's inherited risk for age-related macular degeneration (AMD), the most common form of acquired blindness in the developed world, affecting over 10% of individuals. ArcticDx will use the PBDF investment to undertake studies in support of a planned filing for Food and Drug Administration (FDA) approval for Macula Risk.

Macula Risk detects variations in genetic markers known to predict the progression of early asymptomatic AMD to blindness using a cheek swab sample. The eyesight of individuals who are genetically predisposed to blindness can be saved through enhanced surveillance and early treatment. Macula Risk helps target effective care to those who need it most and relieves others who would otherwise live with uncertainty.

"The investment from OGI will support our filing for FDA approval for Macula Risk," commented Mr. Gregory Hines, CEO of ArcticDx. "We think this approval is an important departure from the growing trend of direct to consumer marketing of genetic tests that have only a weak link to science and are often of no clinical value. Macula Risk stands as the best example of a validated test for a multi-genetic common human disease. Achieving FDA approval will position Macula Risk for wide spread adoption."

The Macula Risk test will be marketed to eye care professionals who manage most cases of AMD in North America. These doctors will offer the test to individuals with the dry form of the disease who have not yet lost vision.

In the industrialized world, AMD is the major cause of uncorrectable vision loss in the elderly, affecting over 2.5 million people in Canada and over 25 million people in the USA. Age?related macular degeneration is generally a disease of the elderly with the worldwide incidence of the disease growing from one in ten people over the age of 60 to more than 1 in 4 people over the age of 75. Macular degeneration is more common than Parkinson's disease, Alzheimer's disease, breast cancer and prostate cancer combined.

"Application of genomics technologies is opening the door to an era of personalized medicine in our approach to preventing, detecting and treating human disease," commented Dr. Christian Burks, President and CEO, OGI. "We are particularly pleased to be investing in a company that grew out of applied research funded by Genome Canada through OGI."

The funded work will focus on a cohort of patient samples who had early stage AMD in the Age-Related Eye Disease Study (AREDS), a large eye survey carried out by the American National Eye Institute. These patients were followed over a five-year period to determine progression of the disease. The ArcticDx team will undertake a prospective study on this cohort to evaluate use of Macula Risk in predicting which patients will progress to wet AMD (the late form of AMD) and which will not.

OGI's PBDF program invests in opportunities ? based in genomics, proteomics or associated technologies ? that fall in the proof-of-principle (validation) phase of research and that have the short-term potential to secure a significant next step towards the marketplace. Previous recipients have included Ontario universities, research institutes and companies.

CIRM to dole Out $72M to Advance Research and Recruit Stem Cell Scientist

2010-10-23T19:41:00.000-07:00

The California Institute for Regenerative Medicine (CIRM) approved funding for 19 awards worth $67 million under the Early Translation II Awards program. The 29-member governing board also voted to approve the second Research Leadership Award of $4.8 million, given to aid in recruiting Peter Coffey, D.Phil., from the University College London to the University of California, Santa Barbara.

The Early Translation II Awards are the second of what CIRM expects to be a 12- to 18-month award cycle for translational research grants. The funded projects are expected to either result in a candidate drug or cell therapy or make significant strides toward such a candidate.

“We are looking for ways to complement our leading edge of stem cell-based treatments for patients, and these projects will load our frontline portfolio with promising studies on autism, muscular dystrophy, Canavan disease, and liver disease,” says Alan Trounson, CIRM president.

The awards went to one for-profit and 11 not-for-profit institutions. The for-profit company iPierian will take its award in the form of a loan. Three of the awards include collaborators in Germany. The portion of the projects carried out by these collaborators will be supported by the Federal Ministry of Education and Research, the science financing agency in Germany, which will fund up to $15 million for this round of awards.

The $4.8 million grant under the Research Leadership Award program will be spread over six years and will back Dr. Coffey’s research on maturing embryonic stem cells into retinal pigment epithelial cells to treat macular degeneration and other forms of vision loss such as diabetic retinopathy and retinitis pigmentosa. Dr. Coffey is part of a team working toward a therapy for macular degeneration led by Mark Humayun, M.D., Ph.D., at the University of Southern California.

“Recruiting internationally renowned stem cell experts such as Dr. Coffey builds a critical mass of stem cell leadership in California to drive the creation of innovative therapies for patients suffering from chronic disease or injury,” notes Robert Klein, chair of the CIRM governing board.

Vitamin A pill could save sight

2010-10-18T06:02:00.000-07:00

By Fiona Macrae
A drug based on vitamin A could prevent millions from going blind as they get older, doctors believe.

The treatment was able to stop the most common cause of blindness in old age during trials.

Researchers behind the drug, fenretinide, found it halted the advance of age-related macular degeneration, for which there is currently no cure.

They targeted the most prevalent form of the condition, known as ‘dry’ AMD, which is caused by the deterioration and death of cells in the macula – the part of the retina used to see straight ahead.

The disease robs sufferers of their sight by creating a blackspot in the centre of their vision.

It can make it impossible to carry out everyday tasks such as reading, driving and watching television.

While the less common ‘wet’ form can be treated, nothing can be done to help the bulk of patients.

The U.S. research studied fenretinide, which is derived from vitamin A, the vitamin found in carrots, and which was originally designed to tackle arthritis.

Almost 250 men and women with dry AMD took a fenretinide pill a day or a placebo.

In the highest dose, the drug halted visual deterioration after a year. This suggests that while it was unable to do anything to stop cells that were already damaged from dying, it protected healthy cells. Although the research is still preliminary, it offers promise of a treatment for the disease.

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It affects millions across the world and 300,000 Britons. The number of UK sufferers could more than treble to one million within 25 years as the population ages.

Dr Jason Slakter, of New York University School of Medicine, said: ‘There are currently no effective treatments for dry AMD and the need for finding one is grave.

‘Our study wasn’t designed to give a final answer.

‘It was designed to see if there was a biological effect and if the drug was working in the way we’d expect and to find out if it was well tolerated by patents.

‘I think we answered all of these points favourably. The bottom line is that I am excited about doing more studies.’

Further, larger trials are planned for the end of next year.

If the drug lives up to its initial promise, it could be in widespread use for dry AMD by 2015.

The treatment works because in normal circumstances the eye needs vitamin A to help it see. The retina naturally uses the vitamin and is helped to do so by a compound called retinol binding protein, or RBP.

However in some patients, the vitamin can produce poisons that kill the delicate cells, leading to loss of vision.

Fenretinide acts as a decoy, attaching itself to the RBP and stopping vitamin A from causing harm, the American Academy of Ophthalmology’s annual conference heard.

Wet AMD, in which tiny blood vessels bleed into the retina, is less common, but progresses more rapidly, with central vision being lost within months of diagnosis.

Caught early enough, wet AMD can be stopped in its tracks by a technique called photodynamic therapy, which uses a light-activated dye to destroy abnormal blood vessels. Drug treatments are also available.

Fenretinide also halved the odds of the patients, who already had dry AMD, going on to develop wet AMD.

A spokesman for the research team said: ‘Years of use of fenretinide to treat cancers, rheumatoid arthritis have shown it to be safe and well-tolerated.’

Prizes Honor Studies in Vision Loss

2010-10-10T06:39:00.000-07:00

Posted by admin

NEW YORK – Three scientists have won prestigious medical prizes — one for devising a treatment for a major cause of vision loss and two for laying the groundwork for an explosion in obesity research.

The Lasker Awards, worth $250,000 apiece, will be presented Oct. 1 by the Albert and Mary Lasker Foundation. A fourth scientist is being honored for decades of statesmanship in biomedical sciences.

The clinical research award goes to Dr. Napoleone Ferrara, 54, of the biotech company Genentech in South San Francisco, Calif. He is honored for discovering a protein called VEGF in 1989 and using it to develop a treatment that significantly improves sight for people with a devastating type of age-related macular degeneration.

More than a million people worldwide have been treated based on Ferrara’s research, the Lasker foundation says. The type of age-related macular degeneration his research addressed — “wet” as opposed to the more common “dry” form — accounts for a tenth or more of the 25 million to 30 million cases of AMD worldwide.

Two drugs based on Ferrara’s VEGF research, Lucentis and the cancer medicine Avastin, are used for wet AMD, attacking it by discouraging the formation of an abnormal growth of blood vessels behind the retina.

The Lasker prize for basic research is shared by Douglas Coleman, 78, of the Jackson Laboratory in Bar Harbor, Maine, and Jeffrey Friedman, 56, of Rockefeller University in New York. They are honored for the discovery of the hormone leptin, which helps regulate appetite and body weight.

In the 1970s, Coleman showed that mice have some sort of appetite-suppressing substance in the blood. Friedman identified the substance in 1994 and named it leptin. People have leptin too, and the research opened new avenues for exploring the biological basis of human obesity, the foundation said.

A Lasker award for special achievement in medical research goes to Dr. David Weatherall, 77, of Oxford University. He is honored for 50 years of “international statesmanship in biomedical science,” including his research on an inherited anemia called thalassemia.

The Lasker foundation was established in 1942. Albert Lasker was an advertising executive who died in 1952. His wife Mary was a longtime champion of medical research before her death in 1994.

Portable Macular Degeneration (AMD) Early Detection & Screening Device

2010-10-04T09:20:00.000-07:00

Health Research Sciences has developed a new portable device allowing early detection of the leading cause of blindness in the US; Age-Related Macular Degeneration (AMD) and Diabetic Maculopathy. This inexpensive and portable device will be an integral part during the next few years in the fight to reduce AMD in the US.

Lighthouse Point, Florida September 30, 2010. Health Research Sciences introduces a new approach for testing macular function with the purpose of early detection of Age-Related Macular Degeneration (AMD), Diabetic Maculopathy and other retinal pathologies. The MDD-2 Macular Degeneration Detection & Screening Device has a unique, hand-held design that measures photostress recovery and solves the problem of inconsistent macular function testing.

The MDD-2 provides reproducible measurements of macular function (precise photostress recovery times) which are documented in a concise format for health professional interpretation. The MDD-2 also permits monitoring of central retinal health over time and can warn of deterioration in function at an early stage. Over 10 million Americans suffer from vision loss due to Macular Degeneration and approximately 4 million Americans are at risk for vision loss from Diabetes and further that these vision disorders cost all Americans over $1 billion annually.

The MDD-2 enables Ophthalmologists, Optometrists, Primary Care Physicians and Endocrinologists to easily and efficiently measure macular function for the purpose of early detection of AMD, Diabetic Retinopathy and other central retinal diseases. The test may be administered by a trained technician/assistant and takes approximately 4 minutes to complete. Results are available immediately and easily interpreted by the physician.

“As Professor of Ophthalmology and Pathology, Johns Hopkins University, School of Medicine, I am very concerned about the need for early detection of Age Related Macular Degeneration (AMD) and Diabetic Retinopathy in the United States. I believe that dark adaptation and photostress recovery measurement are both effective tests for evaluating the function of the macula, detecting macular degeneration and diabetic retinopathy at an early stage.”

Mark O.M. Tso, M.D., D. Sc.

Shark Liver Oil and Cartilage could provide Rescue

2010-09-18T02:25:00.000-07:00

By Debbie Nicholson

Sharks are labeled with a bad persona. Mainly due to movies like "Jaws" where they go around and chomp down for a nightly feast on any human or animal they can find. There are one million slaughters going on each year on this creature. However, these creatures of the sea have the ability to aide in certain medical conditions such as anemia, brain bleeding and cancer.

Scientists for decades have been studying the shark, well at least his cartilage. They believe this creature has something that can offer the medical community especially in the treatment of cancer. It is a known fact that sharks hardly ever get cancer. There must be something in their bodies that aide in protection from this disease.

The theory of the shark cartilage and cancer among most of the scientific community is having to do specifically with the composition of the cartilage. For one thing cartilage cannot grow cancer due to the fact it has no blood vessels. The theory is that the cartilage manufactures elements that barricade the growing of new blood vessels that would feed on the tumor. So by using the cartilage to treat the tumor the blood vessels then should be stopped from developing on the tumor.

A study was performed to scientifically prove or disprove the theory of shark cartilage. Nine patients had participated in this study. When the study had been completed the evidence indicated that seven of the nine patients who had advanced cancer there was an 87% positive response from the treatment. It is important to note that no other treatment was applied during this study.

The evidence laid out had shown the following results (in brief form here after seven weeks of treatment and all patients were diagnosed as terminal)

A few results:

Female patient stage three uterine cancer going into bladder. Radiation had no effects on the tumor. After seven weeks of the cartilage the tumor reduced in size by 80% and after eleven weeks the tumor had gone and so did her pain. The only remaining factor was scar tissue.

Female with vaginal hemangioma in size of 5"x 5" after hysterectomy and partial vaginectomy along with radiation. Heavy bleeding was life threatening complication. At seven weeks tumor reduced by 60% and bleeding had stopped. At eleven weeks tumor size was 3"x 3" with further treatment it was stated tumor would appear to decrease.

Male stage three cancer on back of right thigh. After nine weeks of cartilage therapy surgery was done. It was noticed that 60% of the tumor was dead and surgically removed.

The summary of this research had indicated that further research was still required but shark cartilage treatments had displayed promise.

Studies on shark cartilage are still being conducted however, these studies are extremely expensive. At the same time environmentalists are advocating for the shark and making the fact known that the shark population has decreased significantly in the prior fifteen years due to over fishing and the ever on going demand for shark products.

The compounds of the shark cartilage are being tested by a few pharmaceutical companies. If developed it would only be able to be available by prescription and it is stated the cartilage is coming from those sharks who have been slaughtered for meat.

Shark cartilage in research has shown it can help alleviate arthritis symptoms. In all reality scientists had determined it is one of the main components in the shark cartilage which is chondroitin sulfate that is the magic behind the alleviation. To make a note the supplements which are sold in health food stores usually come from cows and that of sharks.

Shark cartilage has demonstrated benefits in patients with arthritis. It decrease joint pain and inflammation which enabled patients to use less pain relievers. Good news is a lot of persons who use it in small doses have no major problems. Some can have side effects which include nausea, vomiting, cramping, can lower blood pressure and raise sugar levels. Pregnant women, children and those recovering from surgery are advised against using the product. It has been validated for use in osteoporosis.

Shark cartilage has also been noted to be used for psoriasis, healing wounds, retina damage due to diabetes and inflammation of the intestines. The FDA has given the cartilage "Orphan Drug Status"for renal cell carcinoma. This law allows drug pharmaceuticals special incentives to study drugs for rare conditions.

Currently there has been no reported cases for drug interactions of this product. Doses are dependent on a variety of factors such as age, health and other conditions. There is no current information for proper dosage of this product. Follow directions on label and consult health practitioner before using this product.

Shark liver oil is also being used to treat health conditions. The liver oil is either brown or yellow in appearance. Fisherman for a very long time have used the oil for health treatments. The oil is an abundant source alkyiglycerols which just possibly contain anti-cancer elements. There are currently two other chemicals in the oil which are being studied for cancer they are squalene and squalamine.

Shark liver oil is vastly used in northern Europe as one of the conventional cancer treatments. However, in the United States it is sold as a dietary supplement. Current research is aiming at the components of the oil alkyiglycerols, squalene and squalamone. Past scientific studies have demonstrated the oil possibly has anti-cancer reactions on tumors in animals. Clinical trails based on if it works in humans are currently being studied.

We do know that shark liver oil aides in heightening the immune system, fighting infections, in cancer treatments (northern Europe) and decreases side effects of conventional cancer treatments.

The theory of the alkyiglycerols provide benefits in several different ways. It has been proposed that when fighting cancer they kill off the tumor cells indirectly. Advocates allege they stimulate the immune system by activation of immune cells (macrophages) that eat germs that are trying to penetrate along with damaged cells. The other way is that they have the ability to lessen side effects from chemotherapy and radiation therapy. This is due to the fact they can guard the cell membrane.

Due to the ability to heighten the immune system, there are claims that they provide protection against colds, flu, chronic infections, asthma, arthritis and AIDS.

Previous studies have demonstrated that squalamine can slow down the growing of tumor blood vessels. Advocates lay claim that it just possibly could treat cancer either independently or with chemotherapy. It is currently in studies for macular degeneration, eye condition in which ends in vision loss. Squalene is advocated to having cell protection ability which in turn could possibly lessen side effects that occur from chemotherapy.

All claims to shark liver oil are currently being researched.

Based on how the oil is prepared for commercial use it possibly can be loaded with omega 3 fatty acids and Vitamin A. The oil has been used in already in some moisturizing skin creams and lotions. Just to note some cosmetic companies have removed the ingredient over concern for the decline in the shark population.

The shark liver oil is being sold in capsules and liquid forms. You can purchase it at many of the health food stores and over the internet.

To clarify a few points in the shark liver oil. There is no current evidence that the supplement are effective to treat cancer. There have been a couple of studies that did present some benefit to women who were having radiation therapy for cervical cancer. There has been no other confirmed research in this area since 1980.

Recent studies have demonstrated squalamine has lessened the amounts of lung metastases, tumors in which spread to lungs from a primary cancer which is elsewhere in the body and this was found in animals. Studies conducted early in humans did show it can be used safely with chemotherapy. It is still not determined if it does shrink the tumor or prolongs survival of patients. It is undergoing studies with other treatments for lung and prostate cancers.

Some side effects include nausea and upset stomachs have been noted. In animal studies it had shown it could raise blood pressure. If you are allergic to seafood you could have a reaction.

The dosage for shark liver oil is also undetermined at this time so it is advisable to talk with your practitioner first.

Please do not use this product on its own current merit solely. It is used to aide in other treatments and best used with the advice of your health care practitioner.

AstraZeneca joins UCL to find stem cell cure for diabetic blindness

2010-09-13T06:44:00.000-07:00

* Julia Kollewe
12 September 2010

AstraZeneca and University College London (UCL) will announce a research partnership tomorrow to develop medicines that use stem cells to repair damaged eyesight in people with diabetes.

Under the three-year deal funded by the drugmaker, researchers from AstraZeneca will team up with scientists at the UCL Institute of Ophthalmology to work on new medicines that use the regenerative capacity of stem cells. They hope to come up with a compound in three to five years, which could then undergo clinical development and possibly be on the market in 10 years' time.

Dr Marcus Fruttiger of the UCL Institute of Ophthalmology, who is leading the project, said: "These tools could be used either to manufacture transplantable material or to directly stimulate new cell growth in the eye to help restore or improve the vision of those with diabetic retinopathy [DR]."

DR is now the most common cause of vision impairment or blindness among western people of working age. The majority of patients with type-1 diabetes, which occurs when the body produces no insulin and often develops during the teenage years, will suffer eyesight problems and about 20%-30% will become blind. Moreover, at least 50% of patients with type-2 diabetes – the far more common type of diabetes, which occurs when the body produces too little insulin or when cells in the body do not react properly to insulin – will also develop retinopathy over time.

With the rapid spread of type-2 diabetes, which is linked to obesity, the need for a retinopathy treatment will grow as more than 438 million people are expected to suffer from diabetes by 2030. A study published this year by Oxford University predicted that eight out of 10 men and almost seven in 10 women will be overweight or obese by 2020. It forecast a 98% rise in obesity-related diabetes by 2050.

Alan Lamont, director of sciences and technology alliances at AstraZeneca. said: "We're getting very keen on the whole area of regenerative medicines and they will be part of our research development over the next few years." He said the collaboration aimed to come up with a treatment that could be administered to the back of the eye to repair damage locally.

AstraZeneca's US rival Pfizer also has a partnership with Professor Pete Coffey of the UCL Institute of Ophthalmology, for another eye condition, macular degeneration. Coffey said: "It's great that 'Big Pharma' is considering regenerative medicines as a serious possibility." He added: "This is British science being developed into a commercial entity with the pharmaceutical industry. It's a good example why the government shouldn't cut funding for biomedical research."

While this is the first time that AstraZeneca has worked on medicine for retinopathy, diabetes has been an area of focus. The company has a new diabetes treatment on the market called Onglyza, which was developed with Bristol-Myers Squibb, and the companies are developing a second diabetes drug that could be submitted to regulators for approval later this year.

Federal stem cell ruling blocks Yale scientists

2010-09-04T12:27:00.000-07:00

By Rachel Gilmore

For two decades, Lawrence Rizzolo, the director of medical studies at the Yale School of Medicine, has been working toward a project that aims to transplant young, healthy retinal cells to replace diseased tissues in the eyes of patients who are going blind.

But now Rizzolo fears he may have to delay, or even stop, his research because of last week’s ruling by a federal judge that prevents federal funding for studies involving embryonic stem cells, the building blocks for human organs and tissues that Rizzolo needs for his project.

Rizzolo had applied for a grant from the National Institutes of Health to replace his funding from the nonprofit International Retinal Research Foundation, which ends in December. Rizzolo also has a three-year state grant from Rocky Hill, Conn.-based state holding company Connecticut Innovations, but he says he cannot continue his research without the federal funding.

Rizzolo’s laboratory is one of about a dozen facilities on campus that use stem cells. Haifan Lin, director of the Yale Stem Cell Center, said he did not yet know how the moratorium will affect Yale researchers.

“We’re all waiting for clarification on the implications of the judge’s ruling,” University President Richard Levin said.

But frozen funding could lead scientists to lose their jobs. Rizzolo said that although a fourth researcher will join his laboratory in October, he may soon have to fire his workers because the grants and not the University pay for his researchers’ salaries.

Although the U.S. Department of Justice has filed a motion seeking to delay the federal judge’s ban on funding, the relief would only be temporary, NIH spokesman Don Ralbovsky said. The Justice Department declined to comment Thursday.

Opponents of embryonic stem cell research have hailed the ruling.

“The American people should not be forced to pay for experiments — prohibited by federal law — that destroy human life,” said Steven Aden, the legal counsel for the Alliance Defense Fund, which advised the party that brought the lawsuit to court.

Most labs at Yale’s Stem Cell Center are supported primarily by state funds, which are not affected by the ruling, said Diane Krause, the center’s assistant director. But, she explained, those state grants were meant to be a springboard for acquiring federal funding.

“Discontinuation of NIH funding of work with human embryonic stem cells could be a disaster,” she said.

School of Medicine Dean Robert Alpern agreed, saying that halting the stem cell research would be a “loss to society.”

Krause and other Yale researchers met Aug. 26 with Connecticut attorney general and U.S. Senate candidate Richard Blumenthal LAW ’73, who told the News this week that he plans to file a brief in support of the appeal.

“It is incredibly important for our scientific and legislative leaders to come together and solve this issue quickly,” Blumenthal said in a statement. “We have already lost so many years of work to backwards-looking and bureaucratic federal policy.”

Linda McMahon, his Republican challenger for Chris Dodd’s Senate seat, also supports stem cell research, according to her website. The McMahon campaign did not respond to multiple phone requests for comment this week.

Even if the Justice Department successfully delays the ruling, NIH has not said whether it would accept new applications. That would be a problem for Yibing Qyang, an assistant professor of cardiology at the School of Medicine who currently has a $95,499 federal grant and had planned on applying for another in October.

“I cannot live without federal funding,” said Qyang, who is priming stem cells to become healthy heart cells in patients with heart disease.

Yale has received at least $17 million in state funding from a $100 million stem cell research pot funded in part by tobacco taxes. It also received $4.9 million in NIH stem cell research grants in 2009 and 2010. NIH gave $123 million to researchers in fiscal year 2010 for embryonic stem cell research, Ralbovsky said.

Rizzolo studies eye tissues called retinal pigment epithelia. Many eye diseases — including macular degeneration, from which more than 10 million Americans suffer — affect these tissues, which function as a support for the retina, the part of the eye responsible for sight. Doctors have tried to transplant retinal and epithelial cells to combat these diseases. But most of the transplants fail because they are risky and the patients who choose to undergo them are usually almost blind. Patients in the early stages of macular degeneration are unlikely to attempt a transplant; Rizzolo said he hopes that his research with stem cells, which he started to use about a year ago, would lead to other, less risky, treatments for the disease.

Rizzolo added that, in the past year, two Yale colleagues had entirely shut down their stem-cell research labs because of funding shortages.

“It’s pretty frustrating when you work so hard to see something go unfunded for political reasons,” he said.

The Yale Stem Cell Center, established in 2006, brings together more than 30 faculty members across the University.

Gene involved in Fuchs Corneal dystrophy is found

2010-08-29T16:59:00.000-07:00

A 13-member research team led by University of Oregon scientist Dr. Albert O. Edwards has found a gene likely responsible for Fuchs corneal dystrophy, an inheritable genetic disorder and leading cause of corneal transplant operations.

Edwards performed a genome-wide analysis comparing patients with and without typical age-related Fuchs, finding an alteration in the transcription-factor-4 gene (TCF4). Fuchs -- pronounced FEWKS or FOOKS -- generally emerges in middle-aged, roughly age 40, and older people.

The discovery appears online Wednesday, Aug. 25, ahead of regular publication in the Sept. 9 issue of the New England Journal of Medicine.

Fuchs emerges slowly with blurred or cloudy vision, tiny bumps known as guttae (GOO-tay) on the cornea's surface and, in severe stages, painful blisters on the corneal surface. The disease affects the endothelium, a thin layer of cells that line the back part of the cornea where changes result in swelling of the cornea and thickening and clouding of the cornea. Guttae are found in the corneas of an estimated 5 percent of people in the United States.

Of those diagnosed with Fuchs, only a small percentage go on to require corneal transplants, said lead author Dr. Keith H. Baratz of the Mayo Clinic ophthalmology department in Rochester, Minn. There are about 40,000 corneal transplants -- about 10,000 linked to Fuchs -- performed annually in the United States, according to the Eye Bank Association of America. It is more common in women than in men, according to the Fuchs Corneal Dystrophy Association.

The discovery won't immediately translate into clinical benefits, but "this is the first step in identifying the pathophysiology of the disease," Baratz said. "Right now, we don't have a treatment for Fuchs dystrophy other than transplant surgery when a patient is at the end stages of the disease. The ultimate goal is to find out how the disease occurs and find a treatment to prevent or slow its progression."

Having the TCF4 gene variation has a huge impact on the risk of Fuchs disease, said Edwards, a senior research associate in the University of Oregon's Institute of Molecular Biology. "It vastly exceeds the risk found previously for the complement-factor-H gene in macular degeneration," he said. "If a person has risk variants involving TCF4, that individual is anywhere from several to a couple of hundred times more likely to have Fuchs disease."

Edwards, in 2005, when at the University of Texas Southwestern Medical Center, was lead author of a study published in the journal Science that identified complement factor H in macular degeneration. That gene discovery tied complement factor H to a five-fold increase of risk to developing macular degeneration, accounting possibly for at least 50 percent of the risk of being affected. The risk impact of TCF4 on Fuchs is much stronger, Edwards said.

While the TCF4 gene has been identified, exactly what occurs to cause a defect is not understood. The researchers found evidence that at least one transcription protein, E2-2, needs more scrutiny. "E2-2 is a transcription factor. It controls gene expression," Edwards said. "The pathway probably contains E2-2 and the protein ZEB1, but we don't really know that yet. We do find variation of expression across this region, so it has something to do with the expression of the gene."

E2-2, important in cellular growth and differentiation, has been implicated in other disease states, including activity that promotes or suppresses cancer. It is expressed in the corneal endothelium. ZEB1, which may be regulated by E2-2, already is thought to contribute to Fuchs.

The study involved the genotyping of 280 Fuchs patients recruited in clinical settings in Minnesota and Michigan. These patients had at least Stage 1 signs of Fuchs or had received corneal replacements as a result of the disease. Their genomes were compared with 410 control patients.

"The real impact of what we've done is to determine the biological underpinnings of the disease," Edwards said. "We've identified a protein that is probably involved, and that will allow us to, hopefully, identify a method to prevent people from losing their vision."

Three other genes previously had been linked to very rare subtypes of Fuchs. In addition, early onset Fuchs has been linked to mutations in yet another gene, COL8A2, but Edwards and colleagues suggest in their paper that this may be a different disease with a different cause.

"This discovery demonstrates the value of excellent clinical phenotyping and a large-scale genetic database of genome-wide association studies (GWAS) to uncover genetic risk factors for many vision-related disorders," said co-author Anand Swaroop, chief of the National Eye Institute (NEI) Neurobiology-Neurodegeneration and Repair Laboratory. "The genetic data used in this study was obtained for GWAS of age-related macular degeneration through a scientific collaboration supported by the NEI."

International Stem Cell Corporation Formalizes Stem Cell- Based Eye Care Programs Into Cyovis

2010-08-23T06:55:00.000-07:00

Article Date: 22 Aug 2010

International Stem Cell Corporation (OTCBB:ISCO), announced that its stem cell therapeutic programs focused on protective, transparent corneas (CytoCor™) in the front of the eye and the light-sensitive retinal tissue (CytoRet™) in the back of the eye will be formalized into a new business unit, Cytovis™. Together these programs will leverage external and internal development, regulatory and commercial expertise in cellular ophthalmology to form a focused portfolio of complementary product candidates designed to address high unmet medical needs with apparent pharmacoeconomic and quality of life benefits.

CytoCor is the brand name for ISCO's corneal tissue that can be derived from the company's proprietary parthenogenetic stem cells or commonly used embryonic stem cells. Research and development with partners Absorption Systems in the US, Sankara Nethralaya in India and Automation Partnership in the UK continues for the purpose of optimizing the tissue for transplantation in the 10 million people worldwide suffering from corneal vision impairment and as an alternative to the use of live animals and animal eyes in the $500+M market for safety testing of drugs, chemicals and consumer products. ISCO's goal in the coming months is to establish funding and infrastructure in India for accelerated development of CytoCor for the therapeutic application and to advance and implement the chemical testing application with partners in the US and Europe.

CytoRet is the brand name for ISCO's stem cell-derived retinal tissue. ISCO is using its parthenogenetic stem cells to develop individual retinal pigmented epithelial ("RPE") cells and layered retinal structures internally and in collaboration with the laboratory of Dr. Hans Keirstead, Professor of Anatomy and Neurobiology at the University of California, Irvine. ISCO recently commenced a new research collaboration with UC Irvine to launch the next phase of its retinal studies with that institution, including preclinical trials. Potential therapeutic applications include retinitis pigmentosa, an untreatable inherited disease affecting about 100,000 Americans, and the dry form of age-related macular degeneration, a major cause of blindness in the elderly of the Western world. ISCO's goal is to establish functional proof of concept for RPE cellular therapy in models of human disease in the next twelve-eighteen months.

Jointly referred to as Cytovis ("cyto" for cellular, "vis" for vision), these two cellular ophthalmology programs share a number of features and benefits. First, with the aging of the population worldwide and the growing number of work-related eye injuries in India, China and other major countries, the market opportunity is growing steadily. Second, there are strong pharmacoeconomic and quality-of-life rationales for full or partial vision restoration or delay of vision impairment diseases. Third, delivery of cells and tissues to the confined anatomy of the eye inherently provides for better safety and efficacy than, for example, the systemic circulation or the central nervous system. This will likely result in lower regulatory barriers and shorter and less costly development paths compared to that of anatomically deeper and more widespread diseases. Fourth, a number of eye diseases cannot be treated with surgery or traditional small molecule or protein therapeutics, yet cell and tissue therapy is proven to work but currently limited by availability of safe and sufficient cells and tissue from human donors. Finally, eye care development programs like CytoCor and CytoRet share a number of regulatory, development and commercial aspects that make it feasible for a relatively small team to produce substantial clinical outcomes and achieve competitive presence in the marketplace alone or in collaboration with dedicated partners.

Brian Lundstrom, ISCO's President, says: "ISCO's proprietary parthenogenetic stem cell technology continues to form the foundation for the company's long term regenerative medicine therapy programs. In the nearer term, CytoCor and CytoRet's unique benefits in the field of cellular ophthalmology offer the potential for partnering and funding at a relatively early stage. Combined with the current and future revenue of Lifeline Cell Technology and the revenue potential of Lifeline Skin Care, scheduled for launch in the 4th quarter, Cytovis adds significantly to ISCO's diversity and value creation potential for its investor base in a cost-efficient fashion."

Source:
International Stem Cell Corporation

Macular Degeneration and Heavy Metals

2010-08-18T07:28:00.000-07:00

By Jannette Barrett

What Is Macular Degeneration?

Macular Degeneration is a condition that affects the macula part of the retina of the eye resulting in a disturbance to central vision. Although the exact etiology of the disease is unknown, it is believed that deterioration of the retina leads to a breakdown in the transmission of signals to the brain from the nerves and receptors of the eye. When the signals are unclear, the brain cannot correctly interpret the information it receives and there is a loss of the detail that allows us to read, recognise people, perform manual work or manage fine tasks such as threading a needle. A person with macular degeneration may experience blurred or decreased central vision, blind spots, wavy lines instead of straight and size distortion.

There are two types of macular degeneration, wet and dry.

The onset of wet macular degeneration occurs when abnormal blood vessels, which have grown under the centre of the retina, bleed or leak and scar the retina. Macula damage may occur rapidly. It is not uncommon for wet macular degeneration to start in one eye and effect the other at a later time.

Dry macular degeneration, which is the most common form, results from a gradual breakdown of cells in the macula leading to blurring of central vision. The onset of dry macular degeneration can be detected early by an optometrist because of the presence of small, yellowish spots, called drusen, at the back of the eye. However, people who have drusen, may not have visual impairment or related symptoms. When dry macular degeneration advances due to damage to the retina and nerves, vision loss will occur.

Macular degeneration is treated by laser surgery, photodynamic therapy where a drug is injected that destroys newly formed, abnormal blood vessels or injections, however, none of these treatments can restore the vision that has already been lost.

Risk factors

There are a number of identified risk factors associated with AMD. Family history and age are thought to be the most common risk factors. People with outdoor occupations and continuous exposure to sunlight may also be at risk, particularly if their skin is lightly pigmented. Women seem to be at a greater risk than men. There are also environmental and behavioural factors such as smoking and obesity. Research cited below shows that a build up of toxic heavy metals can damage eye health.

Research

The National Institute of Health and the National Eye Institute in the US, published the results of a random study of people with moderate and advanced AMD in the Archives of Opthalmology in 2001, entitled the Age-Related Eye Disease Study. The study reported that a significant slowing of disease progression and preservation of sight could be achieved by taking dietary supplements containing high-dose antioxidants and zinc.

Research published by Erie et al in 2005 in the American Journal of Opthalmology, measured the concentration of toxic heavy metals in the fluids and tissues of human eyes. Concentrations of lead, cadmium, mercury, and thallium in ocular tissues, ocular fluids, and blood were found in the autopsy of 30 eyes from 16 subjects. The study concluded the presence of lead and cadmium which had accumulated in the tissues and retinal pigment epithelium and choroid. Further study into the toxicity of these heavy metals and their possible role in eye disease was recommended.

What Can We Do?

In addition to the medical treatments mentioned above, there are a number of common sense things we can do to help prevent the onset of macular degeneration.

In order for high-dose antioxidants and zinc to be effectively absorbed into the body and to protect the eyes from heavy metals, it is firstly essential to detoxify the body. Published clinical trials have shown that when removing heavy metals and toxins, including pesticides and herbicides from the body safely and effectively, supplements will be more readily absorbed, the immune system may function more efficiently and normal blood pressure may be more easily maintained. Eating a healthy diet, including green leafy vegetables and fish, is also essential to good eye health. A healthy diet will help with weight control as will some regular exercise. Giving up smoking is critical for eye health.

Some people also believe in the benefit of eye exercises to increase eye health. Firstly move the eye slowly from side to side, then from top to bottom a few times. Move the eyes in a circular motion, then reverse a few times. Finally, raise your finger level with your nose and focus there for a time, then focus on something in the distance.

Remember the most important step, to take a daily detoxifying shower on the inside to give your eyes the maximum chance for sustained health. Your body will love you!
Author Resource:- Jannette has researched health and well being issues for the past 20 years and holds a Bachelor of Applied Science in Health Promotion. Healthy eating, regular meditation, moderation in everything and taking the correct supplements can make an enormous improvement to the quality of our lives.

The Best 9 Omega-Fish Oil Benefits

2010-08-09T06:26:00.000-07:00

“A huge amount of studies show that, not only are the benefits of fish oil numerous, many of them are really very amazing! It seems sometimes like new research is being produced all the time, as researchers and physicians learn even more about how and why it is indeed effective. The omega-3 fatty acids found in fish oil are “good fats” that are vital to health. They are crucial for our health but our bodies can’t produce them – you have to get them through diet.

Here are some proven fish oil health benefits that should convince you to eat more oily, wild-caught fish and begin taking a highly refined fish oil supplement in the event you’re not at present!

Reduces Pain & Inflammation

Omega-3s possess a great anti-inflammatory impact. Research trials suggest that diets rich in omega-3s (and low in the pro-inflammatory omega-6s) may benefit people with inflammatory conditions — anything that ends in -itis!. Omega-3 additionally has been used to effectively treat neck, back and menstrual pain, allowing study patients to cut down their particular consumption of NSAID medication.

Promotes Heart Wellness & Protects Against Heart Attack and Strokes

Fish oil continues to grow in research reputation as a key promoter of heart health. According to the American Heart Association, fish oil is effective in lessening the incidence of heart disease and aids in reducing risk factors such as high cholesterol and high blood pressure. Research studies of heart attack survivors have discovered that daily fish oil capsules drastically minimize the risk of death, additional heart attacks and stroke. Omega-3s also reduce blood triglycerides, help correct irregular heartbeats, and can help prevent and treat atherosclerosis by preventing the formation of plaque and blood clots, which typically clog arteries.

Ensures Healthy Joints and Reduces Arthritis Symptoms

The omega-3 fatty acids in fish oil reduce tenderness in joints, pain intensity and morning stiffness caused by rheumatoid arthritis. In fact, several test tube studies have shown that omega-3s actually lessen the action of enzymes that break down cartilage. More than 13 published research trials have shown that fish oil supplements are very effective at treating rheumatoid arthritis. Fish oil has helped those suffering from RA to reduce their need for pain medicine.

Supports Happy Mood & Emotional Wellness

In nations where fish makes up a significant part of the diet, nationwide rates of depression are lower. So, it’s not surprising that studies have shown that fish oil capsules can alleviate the symptoms of depression, bipolar disorder and psychosis. Numerous clinical trials have found that participants that took omega-3s in addition to prescribed anti-depressants had a larger improvement in symptoms than those who only took antidepressants, with subjects experiencing a stabilizing effect and less mood swings. Studies have also demonstrated that, when prisoners were administered omega three fatty acids, there was a significant drop in hostile behavior. Omega-3s also appear to lower the risk ofpostpartum depression.

Enhances Mental Focus & Long-Term Cognitive Functioning

Did you know that omega-3s, especially DHA, are highly concentrated in our brains? They’re important for optimal cognitive (brain memory and performance) and behavioral function, as well as normal growth and development. Studies demonstrate that omega-3s may help in maintaining adequate cognitive functioning and possibly in avoiding or delaying the onset of Alzheimer’s disease. We also now know it’s incredibly necessary that pregnant women get adequate DHA, which is required by the developing fetus — during the third trimester of being pregnant, the brain of the fetus grows at a rate of a quarter million new neurons every 60 seconds! Children are also aided by omega-3 intake, as many studies show that omega-3s enhance learning, concentration, reading and vocabulary skills. Countless studies have even shown benefits in treating ADD.

Promotes Vision Wellness

Studies show that people with a greater omega-3 consumption appear to have a decreased risk of Dry-Eye Syndrome and developing AMD, or age-related macular degeneration. Early research also shows that fish oil supplements aid in lessening dry eye symptoms, may help to slow macular degeneration for those already developing it and improves ocular health in general.

Pregnancy, Infant Brain/Vision Development & Reduced Incidence of Childhood Disorders

DHA makes up 15-20% of the cerebral cortex and approximately 30-60% of the retina, so it’s absolutely necessary for normal growth and development of the fetus and baby. Prenatal DHA availability also seems to reduce the chances of childhood allergies and have an effect on motor skill quality, cognitive development and hyperactivity/behavior later in the child’s life. Omega-3s also assist in reducing the risk of low birth weight and premature birth.

Enhances Metabolism of Fat and Weight Loss

According to the National Institute of Health, omega-3s transmit “I’m full” signals to the brain and help quash hunger signals. Research has also shown that omega-3 fish oil improves the effectiveness of exercise in reducing weight. Volunteers who were alloted fish oil with their diet showed greater weight loss as compared to those who didn’t consume fish oil. Exercise along with fish oil had a positive effect on the body shape and body composition of the volunteers. Reduces Risk of Prostate, Breast & Colorectal Cancers Though more research in this area is certainly needed, we now know that the omega 3’s that appear in fish oil assist in the prevention and treatment of testicular, prostate, breast and ovarian cancers. Preliminary studies suggest that taking fish oil everyday can help inhibit the progression of colon cancer in people with early stages of the disease and may even have the capacity to cause apoptosis (cellular death) of cancer cells.

More can be written with regards to the many fish oil benefits. And, as the scientific community and doctors continue to examine omega-3s, you can bet that fish oil will keep making headlines as the ideal source of these essential fatty acids that are so essential to our bodies. Even if you’re currently in great health, a quality fish oil supplement is the fastest, safest way to realize and maintain optimal health!”

Avastin/Lucentis Update 39: And the Controversy Continues

2010-08-04T09:19:00.000-07:00

By Alicia Mundy

Medicare could save more than $500 million annually by using a cheaper Genentech drug to save vision, according to a draft study by federal officials and a University of Miami eye doctor.

The study shows that the cheaper drug, Avastin, is already used in about 65% of Medicare patients with wet age-related macular degeneration and accounts for nearly 60% of their eye injections, compared with about 40% for a more expensive drug called Lucentis. However, Medicare paid $537 million for Lucentis in 2008 and only $20 million for Avastin, according to the unpublished study, which was reviewed by The Wall Street Journal.

The numbers point to a delicate problem for the federal program for the elderly, whose rising costs are often cited as among the biggest long-term factors in the federal budget deficit. Both drugs are made by Genentech, but only Lucentis is approved by the Food and Drug Administration to treat the disease, the leading cause of irreversible blindness among older people.

Clinical trials suggest that Avastin, approved by the FDA to treat some forms of cancer, is also effective in treating the eye disease. Doctors have been "voting for Avastin with their feet," said Philip Rosenfeld, a retina specialist at the University of Miami's Bascom Palmer Eye Institute and one of the study's authors. Some pharmacies take supplies of Avastin and divide it into tiny doses suitable for injection in the eye.

The study, based on data from more than 200,000 Medicare patients, found that Medicare paid on average $42 a dose for Avastin in the eye, compared with $1,593 a dose for Lucentis.

Leading brands under threat

2010-07-26T09:21:00.000-07:00

Ophthalmology encompasses some lucrative markets, but the future of leading brands in AMD is under threat, and while established markets like glaucoma and conjunctivitis have many therapeutic options, diabetic retinopathy remains largely untapped. Key opinion leaders agree there is unmet need in terms of drug delivery methods and dose frequency across ophthalmology diseases.

Highlights

The future of leading brands Lucentis (ranibizumab) and Xalatan (latanoprost) is at risk. Lucentis dominates AMD with 91% market share but the use of currently off-label Avastin (bevacizumab, Roche) is a threat. Xalatan, the gold standard in glaucoma achieved $1.5 billion in 2008 but the drug faces generic erosion after patent expiry in 2011

Diabetic retinopathy and AMD markets show high growth potential. Both diseases are highly prevalent, with 11.5 million cases of diabetic retinopathy, and 7.5 million in AMD, in the seven major markets in 2010. There are few drug treatments for AMD, while no approved drugs for diabetic retinopathy mean this market is untapped.

Key opinion leaders report high unmet need for reduced dosing regimens of existing therapies and an improvement in drug delivery methods. However, any new formulations of existing drugs will have to compete with cheap generics and need to show significant additional benefits.

Reasons to Purchase

*Validate the market potential of particular ophthalmology indications based on prevalence numbers in each of the seven major markets

*Understand the commercial potential of ophthalmic diseases with Datamonitor’s assessment of market and brand dynamics

*Assess the key unmet needs and possible new approaches in the treatment of eye diseases as noted by opinion leaders

Ophthalmology market attractiveness
ophthalmology market definition
Therapeutic sales for ophthalmology disorders exceeded $12 billion in 2008
High growth potential observed in diabetic retinopathy and age-related macular degeneration markets
Age-related macular degeneration shows a high growth rate, and seemingly unsaturated market
Middle Eastern, North African (MENA) and Brazil, Russia, India and China (BRIC) ophthalmology markets are growing rapidly
High pipeline potential in age-related macular degeneration (AMD)
to greater patient compliance
Preservative-free formulations
Therapies with better side-effect profiles
Pipeline analysis of glaucoma treatments
Chapter 3. Age-related macular degeneration
Key findings 70
Definition and classification of age-related macular degeneration (AMD)
Dry (nonexudative) age-related macular degeneration
Wet (exudative/neovascular) age-related macular degeneration
Epidemiology of age-related macular degeneration (AMD)
Over 7.5 million sufferers of age-related macular degeneration in the seven major markets in 2010
estimates over 2.7 million cases of age-related macular degeneration in the US in 2010
Japanese males have higher prevalence of age-related macular degeneration
estimates over 4.3 million cases of age-related macular degeneration across the five major EU markets in 2010
Age-related macular degeneration prevalence is high in India
Age-related macular degeneration prevalence varies in racial groups
Current treatment options in age-related macular degeneration (AMD)
Overview of treatments in age-related macular degeneration (AMD)
Anti-vascular endothelial growth factor (VEGF) therapy
Off-label use of Avastin in age-related macular degeneration
Laser photocoagulation and photodynamic therapy
Other surgical treatments for AMD
Vitamins and lifestyle change are the main treatment options in dry AMD
Age-related macular degeneration (AMD) treatment guidelines Diagnosis of AMD
Treatment guidelines on the management of AMD
Sales analysis of brands in age-related macular degeneration (AMD)
Lucentis drives rapid growth in AMD market between 2004 and 2008
Major brands in AMD therapy
Lucentis (ranibizumab, Roche/Novartis/Alcon)
Macugen (pegaptanib, Eyetech/Pfizer)
Visudyne (verteporfin, QLT /Novartis)
Avastin (bevacizumab, Roche)

Alcon Terminates the Development of Anecortave Acetate in Age-Related Macular Degeneration

2010-07-20T09:25:00.000-07:00

HUENENBERG, Switzerland -- Alcon, Inc. (NYSE:ACL) announced today it has terminated the development program designed to evaluate the benefit of anecortave acetate treatment on the risk for developing sight-threatening choroidal neovascularization secondary to age-related macular degeneration. The decision followed a planned interim analysis of studies C-02-60 A and B that was performed after 2,546 patients had completed the 24 month time point. In this analysis, anecortave acetate showed no effect on the primary or secondary endpoints. In addition to terminating studies C-02-60 A and B, the company also terminated two smaller studies with an identical design that were being conducted in Asia, C-04-30 and C-05-34.

The company continues to study anecortave acetate administered as an anterior juxtascleral depot to reduce intraocular pressure in patients with open-angle glaucoma.

About Alcon

Alcon, Inc. is the world's leading eye care company, with sales of approximately $5.6 billion in 2007. Alcon, which has been dedicated to the ophthalmic industry for more than 60 years, researches, develops, manufactures and markets pharmaceuticals, surgical equipment and devices, contact lens care solutions and other vision care products that treat diseases, disorders and other conditions of the eye. Alcon's majority shareholder is Nestle, S.A., the world's largest food company. For more information on Alcon Inc., visit the company's Web site at www.alcon.com.

Artificial Retina offers new Hope

2010-07-12T16:14:00.000-07:00

TUCSON - There is new hope for millions of people losing their vision. Many are going blind because of age-related macular degeneration and other conditions. But a new device called Artificial Retina has people seeing and believing.

Dean Lloyd is one of 14 people in the United States seeing through an Artifical Retina. He lost his vision in 1974. Lloyd says, "I almost lost all my vision in six months." Then in 2007, after a three hour operation, his sight, though limited, returned. "The beauty of the human brain is when you've had sight at one time, the brain seems to save the images," he said.

The camera on Dean's glasses captures an image and sends it wirelessly to an implant in his eye that stimulates his optic nerve to create an image in his brain. The next generation for Dean's implant is one that could help him see details and faces.

Satinderpall Pannu heads the Artificial Retina project at Lawrence Livermore labs in California. Starting with a silicon wafer and a thin coating of polymer, the disk is processed, electrodes are added and the implant is encased in titanium and gold, "It's a very rewarding feeling. It's amazing to me that technology that we've developed here at the lab can actually restore someone's sight," Pannu said.

Pannu says in 10 years, 50 million people in the world will suffer from blindness that these implants could reverse, "We really would like to take this tech to have a digital camera embedded in your retina and be able to restore your vision completely."

The only clinical trials for the artificial retina in the U.S. are run through a California Company "Second Sight."

Project leaders at Lawrence Livermore say they only have funding through next year. Right now, they're trying to lobby congress to extend the project's 8-million dollar a year budget, to improve the implant.

Miniature Telescope for Eye Approved for Macular Degeneration

2010-07-07T03:19:00.000-07:00

TUESDAY, July 6 (HealthDay News) -- A tiny telescope that's implanted in an eye affected by advanced age-related macular degeneration (AMD) has been approved by the U.S. Food and Drug Administration.
The Implantable Miniature Telescope replaces the natural lens and magnifies an image more than two times, the FDA said in a news release.
The device is meant for people aged 75 and older who have blind spots associated with end-stage AMD. Candidates will be trained with an external telescopic device to see if they may benefit from the implanted product, the agency said.
AMD damages the eye's macula, causing vision loss in the center of the visual field. The condition affects mostly older people, often making it impossible to recognize faces or perform tasks such as watching television, the FDA said. Some 8 million Americans have been diagnosed with the condition, and about 25 percent of those are significantly visually impaired.
The FDA said it's requiring the labeling to warn that the device puts users at greater risk of injury to the eye's cornea.
As a condition of approval, California-based VisionCare Ophthalmic Technologies will conduct two follow-up studies of the device, the agency said.
More information
To learn more about AMD, visit the U.S. National Eye Institute.

Copyright © 2010 ScoutNews, LLC. All rights reserved.
HealthDayNews articles are derived from various sources and do not reflect federal policy. healthfinder.gov does not endorse opinions, products, or services that may appear in news stories. For more information on health topics in the news, visit Health News on healthfinder.gov.

Alimera seek NDA for diabetic macular degeneration drug/device combo

2010-06-30T09:45:00.000-07:00

June 29, 2010 by MassDevice staffpSivida Corp. and Alimera Sciences file a new drug application with the Food & Drug Administration for Iluvien, a drug/device combination aimed at treating diabetic macular degeneration.

pSivida Corp. (NSDQ:PSDV) and Alimera Sciences (NSDQ:ALIM) are seeking a green light from the Food & Drug Administration for a drug/device combination to treat diabetic macular degeneration.

Watertown, Mass.-based pSivida said Alimera, which licenses the Iluvien technology from pSivida, submitted a new drug application to the FDA. The technology is designed to deliver sustained, low doses of flucocinolone acetonide to the retina at the rear of the eyeball.

Alimera asked the federal watchdog for priority review, an expedited process that could bring an FDA response during the fourth quarter, according to a press release.

There are no approved drugs to treat DME, according to pSivida president and CEO Paul Ashton, adding that Iluvien is the company's third product aimed at back-of-the-eye diseases. The first two won FDA approval and are on the market, Ashton said: Retisert, for the treatment of posterior uveitis, and Vitrasert for the treatment of AIDS-related cytomegalovirus retinitis. Both are licensed to Bausch & Lomb Inc.

The company is also working on a treatment for retinitis pigmentosa, which involves the gradual deterioration of the rods and cones that make up the retina. In April Ashton told MassDevice that its Durasert device also uses flucocinolone acetonide, a steroid, to treat the disease.

"What we've done is use a very small insertable drug delivery device to release a steroid directly into the eye that will just provide some protection and slow down the rates of vision loss," he said. "With a condition that takes 20 years to make you blind, if you slow it down by a factor of two, that's pretty good."

The partnership with Alimera has already paid dividends, namely a $15.3 million payment triggered by Alimera's April 21 initial public offering. At the time Ashton told us pSivida planned to use the cash to further develop its product pipeline. If the FDA gives the nod to Iluvien, it would trigger another, $25 million milestone payment from Alimera, plus 20 percent royalties on net profits from sales of the treatment.

For more information go to www.maculardegenerationassociation.org

Researchers create retina from embryonic cells

2010-06-10T06:39:00.000-07:00

By Adrian Galbreth

Researchers in the US have successfully created a retina from human embryonic stem cells, which offers hope to millions with degenerative eye disorders.

Experts at the University of California Irvine created an eight-layer, early stage retina from human embryonic stem cells, which is the first ever three-dimensional tissue structure to be made from stem cells.

Study leader Hans Keirstead of the Reeve-Irvine Research Center and the Sue and Bill Gross Stem Cell Research Center at the facility, said the process also marks the first step towards the development of transplant-ready retinas to treat conditions such as retinitis pigmentosa and macular degeneration, a leading cause of blindness.

"We made a complex structure consisting of many cell types. This is a major advance in our quest to treat retinal disease," he explained.

Recently, German research centre Fraunhofer-Gesellschaft claimed that a new implant made of plastic could soon offer patients the chance to see again without having to wait for cornea transplants.ADNFCR-1853-ID-19804594-ADNFCR

New Drugs for Macular Degeneration

2010-06-02T14:11:00.000-07:00

By Emily Singer

Two genetic studies of people with age-related macular degeneration (AMD)--the most common cause of blindness in people older than 65--made a surprising discovery. Research showed that defects in a gene that is an important regulator of parts of the immune system significantly increased risk of the disease. Scientists have since identified variants in several related genes that also boost risk, and which collectively account for about 50 to 60 percent of the heritability of the disorder.

At the same time that researchers identified the harmful variation linked to AMD, Gregory Hageman, now at the University of Utah, identified a protective variant found in about 20 percent of the population. "That form is so incredibly protective that people with two copies are almost guaranteed not to develop the disease," he says. Hageman founded Optherion, a startup based in New Haven, CT, and investigated how to translate the findings into new treatments. Optherion is now producing large quantities of an engineered version of the protein and doing preclinical safety and effectiveness testing--for example, examining whether the treatment can reduce ocular deposits in mice that lack the protein, says Colin Foster, Optherion's president. He declined to estimate when the company will begin clinical trials of the drug.

Scientists hope that these developments will prove to be an example of the benefits that can arise from a type of genetic study called genome-wide association. The genome-wide studies of macular degeneration were among the first and perhaps the biggest success for the approach, which employs specially designed chips dotted with markers to cheaply detect hundreds of thousands of the most common variations in the human genome. While these chips have allowed scientists to cheaply scan the genomes of many patients and healthy controls, the approach has come under increasing scrutiny in the last couple of years. Even huge studies of thousands of people have failed to identify the majority of the heritability of common diseases, such as type 2 diabetes or Alzheimer's disease.

Decreased antioxidant levels increase risk of age-related macular degeneration with exposure to sunlight

2010-05-27T09:41:00.000-07:00

The journal Archives of Ophthalmology recently reported that having reduced plasma antioxidant levels and increased exposure to sunlight increases the risk of neovascular, or advanced age-related macular degeneration (AMD).

In a recent study (titled the European Eye Study), over 4,400 participants over age 65 were analyzed for the presence of macular degeneration. Their blood plasma was evaluated for vitamins C and E, the carotenoids lutein and zeaxanthin, and the mineral zinc. Each individual also completed a questionnaire regarding their typical exposure to sunlight. This was used to estimate blue light exposure from visible light, which is known to contribute to the development of macular degeneration.

Early stage macular degeneration was detected in 2,182 participants, and 101 had the advanced form of the disease. The research found no association between blue light exposure and early macular degeneration. However, among participants in the lowest quartile (25 percent) of serum vitamin C, zeaxanthin, vitamin E and zinc, exposure to blue light significantly increased the risk of advanced macular degeneration.

Promising new treatment for dry AMD in clinical trials

2010-01-22T21:09:00.000-08:00

Acucela Inc. has announced Phase 2 clinical trials of it’s ACU-4429 for the treatment of dry age-related macular degeneration (AMD). ACU-4429 works by decreasing the levels of toxic products in the eye thus hopefully stopping the advance of dry AMD.

More than 29 million people worldwide are affected by either “wet” or “dry” AMD. The leading cause of the loss of vision in people over the age of 50 is dry AMD. 90 percent of AMD patients suffer from the dry form of AMD. Currently, there are no FDA approved therapies to treat dry AMD which will make the trials of ACU–4429 ones eagerly watched. Anti-oxidants are the only therapy available to slow or halt the progression of dry AMD

Researchers are pleased with the preclinical and early clinical data for ACU-4429. Thus far, it has demonstrated the ability to decrease toxic by-products which have had a part in the progression of dry AMD.

ACU-4429 is administered as an oral, daily pill unlike other therapies for the eyes which can involve the use of injections into the eyes.

For more information go to www.maculardegenerationassociation.org

Laureate Pharma and Iconic Therapeutics complete manufacturing hI-con1 recombinant Fc-Factor VII fusion protein

2010-01-10T23:18:00.000-08:00

Laureate Pharma, Inc., a full-service biopharmaceutical development and protein production company specializing in the development and GMP manufacture of monoclonal antibodies, fusion proteins and other therapeutic protein products, and Iconic Therapeutics, a company focused on the development of treatments for wet adult macular degeneration (wet AMD) and other ophthalmic diseases, today announced the completion of the manufacture of the first GMP lot of hI-con1(TM) recombinant Fc-Factor VII fusion protein.
"We are very excited that Iconic Therapeutics now has material to test this new therapy for patients with macular degeneration and other diseases," said Robert J. Broeze, Ph. D., President & CEO of Laureate Pharma. "This is a testimonial to our strong partnership with Iconic and our expertise in working with fusion proteins." "Due to the unique properties of Iconic's hI-con1(TM) fusion protein product, this project involved very close collaboration between our process-development team at Laureate and Iconic's product-development team," added Michiel E. Ultee, Ph.D., Vice President of Process Sciences.

"With clinical material now in hand, we have moved a giant step forward in our plans for hI-con1(TM). We are excited about its prospects as a novel and powerful approach for the therapy of wet AMD," said Kirk Dornbush, President of Iconic Therapeutics. "We are very pleased with the strong working relationship that we established with Laureate Pharma."

hI-con1(TM) is a recombinant protein intended to specifically attack and destroy pathological blood vessels (PBVs) with no effect on normal blood vessels. Since wet AMD is characterized by the invasion of PBVs into the eye, a drug that destroys these blood vessels could be very useful in treatment of this disease. In addition, hI-con1(TM) is thought to act differently from other wet AMD treatments, which reduce the effects of pathological blood vessel invasion into the eye but do not appear to kill those blood vessels. In studies with mice and pigs, a single injection of hI-con1(TM) into the eye resulted in dramatic reduction of pathological blood vessels.

For more information go to WWW.MACULARDEGENERATIONASSOCIATION.ORG

New research findings may help stop age-related macular degeneration at the molecular level

2010-01-04T09:36:00.000-08:00

Scientists discover the relationship between 2 blood proteins plays a pivotal role in staving off the condition

Researchers at University College London say they have gleaned a key insight into the molecular beginnings of age-related macular degeneration, the No. 1 cause of vision loss in the elderly, by determining how two key proteins interact to naturally prevent the onset of the condition.

In a paper to be published in a forthcoming issue of the Journal of Biological Chemistry, the team reports for the first time how a common blood protein linked to the eye condition reins in another protein that, when produced in vastly increased amounts in the presence of inflammation or infection, can damage the eye.

"By starting to understand these interactions in greater detail, we can begin to devise methods that will ultimately prevent the development of blindness in the elderly," said Zuby Okemefuna, the lead author of the paper to be published Jan. 8.

Age-related macular degeneration, or AMD, is painless but affects the macula, the part of the retina that allows one to see fine detail. One form of the debilitating condition, known as "wet" AMD, occurs when abnormal and fragile blood vessels grow under the macula, leaking blood and fluid and displacing and damaging the macula itself. The second form, "dry" AMD, occurs when light-sensitive cells in the macula slowly break down.

It is believed that both forms start on a common molecular route and then deviate into dry or wet AMD, explained the research leader, Steve Perkins.

"The earliest hallmark of AMD is the appearance of protein, lipid and zinc deposits under the retinal pigment epithelial cells," he said, adding that the yellowish deposits, usually discovered by an ophthalmologist, are commonly known as "drusen."

The researchers studied two proteins involved in drusen formation -- blood protein Factor H and a second blood protein known as C-reactive protein -- and showed that Factor H binds to C-reactive protein when C-reactive protein is present in large amounts, as in the case of infection, to reduce the potentially damaging effects of an overactive immune system.

"In the eye, during the normal processes of aging, cells will die naturally for all sorts of reasons," Okemefuna said. "The blood supply to the eye will bring C-reactive protein with it, and a low level of C-reactive protein activity will enable the normal processes of clearance of dead cells at the retina through mild inflammation. In conditions of high inflammation, the levels of C-reactive protein in the retina will increase dramatically."

Uncontrolled C-reactive protein activity causes damage to the retina, which is followed by more inflammation and then even more damage to the retina, and so forth.

"It's the debris of broken up retinal cells, some of which is caused by this cycle, that is deposited as drusen," Okemefuna said.

The team also found that a genetically different form of Factor H does not bind to the C-reactive protein quite as well as the normal one, making people who carry the modified protein more vulnerable to an immune system attack in the eye and, thus, drusen buildup.

"In normal individuals, further damage to the retina by prolonged exposure to high levels of C-reactive protein is prevented by Factor H. C-reactive protein also prevents Factor H from clumping together and initiating the processes that lead to drusen formation," Perkins said. "Both these 'good' activities of Factor H are much reduced in the genetically different form of Factor H."

While there is no known cure for AMD, existing therapies aim to treat the symptoms and delay progression.

"It is interesting how the interaction of these two blood proteins protects the eye during crisis," Perkins said. "The two proteins also can be involved in a rare and often fatal cause of kidney failure in children. We now are better positioned to begin to work out preventative strategies for these diseases."

For more information go to www.maculardegenerationassociation.org

Scripps Research scientists crack mystery of protein's dual function

2009-12-14T18:43:00.000-08:00

Researchers at The Scripps Research Institute have solved a 10-year-old mystery of how a single protein from an ancient family of enzymes can have two completely distinct roles in the body. In addition to providing guidance for understanding other molecules in the family, the research supplies a theoretical underpinning for the protein's possible use for combating diseases including cancer and macular degeneration.

The research was published in the December 13, 2009 advance, online issue of the high-impact journal Nature Structural and Molecular Biology.

The scientists, led by Scripps Research Associate Professor Xiang-Lei Yang, focused on a molecule called human tryptophanyl-tRNA synthetase (TrpRS), finding that it contains a "functional switch" that enables it to perform two different functions. In one of its forms, the molecule acts to facilitate protein synthesis. In the second form, the same molecule works to inhibit the formation of new blood vesselsan effect that, if successfully harnessed, could be medically useful.

"I'm very excited about these findings," said Yang. "This piece of work provides a very deep mechanistic understanding. It has really shown that the activity of this tRNA synthetase is of biological significance and that it's a good example of the many, many different functions that have been found with the tRNA synthetase family."

One Enzyme, Two Functions

For some time, scientists have known that the aminoacyl tRNA synthetase family is composed of 20 ancient enzymes that attach the correct amino acid to a tRNA as the first step in the synthesis of proteins.

The mystery of the protein family's dual functionality, however, was born about a decade ago, with the publication of a 1999 paper in the journal Science by Paul Schimmel, who is Ernest and Jean Hahn Professor of Molecular Biology and Chemistry and a member of The Skaggs Institute for Chemical Biology at Scripps Research, in collaboration with a member of his lab at that time, Keisuke Wakasugi.

In the 1999 paper, Wakasugi and Schimmel showed that a member of the human aminoacyl-tRNA synthetase family, tyrosyl-tRNA synthetase (TyrRS), did more than adding the amino acid tyrosine to a protein chain during protein synthesis. In addition, a fragment of the protein could function to attract immune cells and to stimulate the growth of blood vessels.

The findings were met with astonishment and some skepticism in the scientific community.

Soon afterward, however, the Schimmel lab showed that another member of the family, TrpRS, also had a dual function. In addition to its role adding the amino acid tryptophan to a protein chain during protein synthesis, a fragment of TrpRS could inhibit new blood vessel formation.

Since that time, there has been considerable therapeutic interest in TyrRS, TrpRS, and other members of the aminoacyl-tRNA synthetase family. As a pro-angiogenic factor, the TyrRS fragment could be useful in diseases where growth of blood vessels is desirable, such as in some forms of heart disease or peripheral artery disease. Likewise, the TrpRS fragment's anti-angiogenic effects could help patients reduce undesirable blood vessel growth in diseases such as cancer and a great many eye diseases that lead to catastrophic vision loss.

In fact, fragments of TrpRS were used as part of a study led by Scripps Research Professor Martin Friedlander that successfully halted the progression in animal models of highly vascular brain tumor and neovascular eye disease (PNAS 2007 104:967-972).

Despite the interest in tRNA synthetases, however, no one has been able to figure out exactly how they perform their different rolesuntil now.

Mystery Mechanism Revealed

In the current study, the research team used a combination of techniques including structural modeling analysis, mutagenesis, and cell-based functional studies to unravel the secrets of TrpRS.

The scientists identified the specific molecular changes that enabled TrpRS to perform one function or another.

In the study, the scientists show that, for its role in protein synthesis, TrpRS is typically in its full-length form. This form of the molecule contains a tryptophan-binding pocket that enables it to bind with the amino acid and shepherd it to where it is needed in protein synthesis.

In the second active form, however, the protein must first be broken into fragments by the body, creating a piece called T2-TrpRS. With the removal of the end of the full-length protein (the N-domain), new grooves in the T2-TrpRS protein fragment are revealed. Containing the now-exposed tryptophan-binding pocket, the grooves fit together with side chains of another molecule, VE-cadherinknown to be indispensable for proper vascular development.

Interestingly, the new study found that tryptophan acts to inhibit of the vasculature function of TrpRS, locking the protein into its protein-synthesis form.

Therapeutic Potential

Yang notes that the therapeutic potential of TrpRS and other tRNA synthetases are particularly good because they normally exist in abundant amounts in the body.

"Naturally, you'd imagine the body's tolerance for such a protein is pretty good," she said, "and we could use the activated form of the molecule."

In addition, Yang points out that TrpRS is intriguing because it does not effect existing blood vessel growth, only new blood vessel formation, reducing the odds of negative side effects from its use.

For more information go to www.maculardegenerationassociation.org

Save your eyesight – stop smoking!

2009-12-03T21:02:00.000-08:00

By Martin Burns

AMD (age-related muscular degeneration) Alliance International is strongly urging smokers to participate in tomorrow`s Great American Smokeout to protect their vision from the effects of macular degeneration.

The leading cause of blindness among people over the age of 50, AMD is two to three times as frequent among tobacco smokers, according to research by JM Seddon last month.

Further research in October by WG Christen revealed that regular heavy smoking can increase the risk of AMD by 144-fold in people with certain genetic backgrounds.

David Herman, AMD Alliance International chairman, said: "We [can] add vision loss to the list of significant and debilitating health risks that are caused by smoking. If you quit today, you can immediately begin lowering your risk of losing your sight to macular degeneration."

Healthcare provider Simplyhealth recently suggested that a diet lacking in fresh fruit and vegetables is a contributing factor to various eyesight conditions.

For more information go to www.maculardegenerationassociation.org

Lutein can Protect Against Macular Degeneration and Promote Eye Health

2009-11-27T11:47:00.000-08:00

As people live longer eye diseases such as macular degeneration and cataracts are on the rise which has a negative effect on eye health. This often robs people of their freedom and quality of life. Age related macular degeneration (AMD) is the leading cause of irreversible blindness in people over 65. AMD occurs when the cells in the central part of the eye, which is called the macular, begin to degrade. This causes loss of sight in the central part of the field of vision, but leaves peripheral vision intact.

It is estimated that as many as 16 million Americans show signs of the initial stages of AMD. To put that into perspective that is roughly twice the population of Los Angeles. While this seems like a very high number the fortunate thing is that 90% exhibit the dry form of AMD which occurs over time and can be corrected with nutrition and lifestyle changes. The dry form of this disease is not associated with blindness, but, if left untreated can progress to the wet form of AMD. This sudden form of the disease leads to blindness in about 10% of AMD patients.

There are a number of factors that are known to lead to the development of AMD. Some of these include age, eye color, gender, exposure to sunlight, smoking, alcohol consumption and heart disease to name a few.

Lutein is a carotenoid found in some vegetables and fruits. It acts as a powerful antioxidant that can protect the eyes from disease and is essential for good vision and eye health. It is not made by the body and can only be obtained by the foods that we eat and nutritional supplements. The problem is that large amounts of fruits and vegetables would need to be consumed to get the required amount of lutein. It is found in green leafy vegetables such as spinach and kale. It is also found in corn and egg yolks. Carotenoids have shown benefits in reducing the risk of cancer, heart disease and eye disease and enhancing the body’s immune system.

Lutein is found in the macular which is the central part of the retina. While it is not a vitamin lutein is an antioxidant that may help to protect the macular tissue from destructive oxidation reactions by eliminating free radicals. It can also filter high energy blue light that has been known to damage the macula and skin.

It was first discovered by a researcher at Harvard University in 1994 that lutein plays an important role in eye health. Since that time there has been significant research on its ability to protect the eyes and is recommended by many eye doctors for their patients.

According to a recent study done by Kemin Foods 91% of eye doctors believe that lutein plays an important role in promoting good eye health. In addition, 58% of those surveyed believe lutein is the best nutrient for promoting long term eye health. This survey consisted of 150 ophthalmologists and 150 optometrists in the United States about their perceptions of lutein.

When the color of one’s eyes starts to fade it is not a result of aging but a loss of lutein. It is used by the eye as a natural antioxidant to eliminate damaging free radicals. Lutein as acts to filter damaging light from the eye. You can think of it as a pair of natural sunglasses.

Assuming that we are getting enough lutein thru diet or nutritional supplementation the good news is that it has the ability to build reserves in the eye to assure long term eye heath. Even for people that are not experiencing any eye problems they can benefit from lutein in preserving the good eye health they already have. Think of lutein as doing the same thing for your eyes as sun block and moisturizer does for your skin. If you start using it when you are young you maintain the healthy appearance of your skin as you age. The same analogy can be applied to your eyesight. When you are 60 it would be nice to have the same vision as when you were 30.

We know that we can not change our age, genetics or gender but there are things in our lifestyle that we can change to protect our eyesight. A few of these are to quit smoking, protect your eyes with sunglasses, limit your intake of alcohol and supplement with lutein.

For more information go to www.maculardegenerationassociation.org

Cataract Surgery Does Not Worsen Age-Related Macular Degeneration

2009-11-16T19:20:00.000-08:00

Fran Lowry

Cataract surgery does not appear to increase the progression of age-related macular degeneration (AMD). Instead, it might reveal pre-existing AMD that had been hidden by the cataract, suggests a new study published in the November issue of the Archives of Ophthalmology.

"There has been a longstanding controversy among clinicians as to whether cataract surgery is contraindicated in eyes with nonneovascular AMD," write Li Ming Dong, PhD, from Stony Brook University School of Medicine in New York, and associates from Johns Hopkins University School of Medicine in Baltimore, Maryland. "A major concern has been whether cataract surgery increases the risk of progression to neovascular AMD in eyes at risk of progression, such as those with intermediate AMD (extensive medium-sized drusen, large drusen, or nonfoveal geographic atrophy)."

The aim of this study was to evaluate the course of AMD during the year after cataract surgery in individuals with preconfirmed nonneovascular AMD.

The investigators analyzed 86 patients with nonneovascular AMD who underwent cataract surgery to note the incidence of neovascular AMD development in the 12 months after the operation. Only 1 eye from each patient was analyzed.

Fluorescein angiography was performed preoperatively, and at 1 week, 3 months, and 12 months postoperatively.

The median age of the patients was 76 years (range, 58 to 92 years); 48% were women, 97% were white, and nearly two thirds were current or former cigarette smokers. The median preoperative visual acuity (Snellen equivalent) was 20/50 (range, ≥20/40 to 20/400).

Photographic documentation of AMD status was done in 71 patients (83%) at the 12-month visit. Sixty-six patients (77%) also completed a clinical examination at this visit.

Neovascular AMD was observed in 9 eyes (12.7%; 95% confidence interval [CI], 6.0% - 22.7%) by 12 months, including 1 that was graded as probable neovascular AMD. Five eyes displayed signs of neovascular AMD at the 1-week follow-up, but the size and location of the lesions indicated that they might have been present before surgery but not visible because of the opacity caused by the cataract, the authors report.

One eye did not have a 1-week follow-up. After excluding this eye, as well as the 5 eyes that showed lesions at the first follow-up period, the rate of confirmed progression to neovascular AMD between week 1 and month 12 decreased to 3 (4.6%) of 65 eyes (95% CI, 1.0% - 12.9%), the investigators report.

The investigators also noted the progression to neovascular AMD in the study subjects' phakic contralateral eyes. They report that neovascular AMD developed in only 1 eye (3%) at 12 months.

Previous Reports Might Be Biased

"Our findings suggest that previous reports of the association or progression of nonneovascular AMD to advanced AMD after cataract surgery could be biased by the absence of immediate preoperative and postoperative fluorescein angiography to rule out pre-existing neovascular AMD or geographic atrophy," the study authors write, adding that a strength of their study — the first to their knowledge — was the use of color fundus photographs and fluorescein angiography in the immediate pre- and post-cataract surgery setting.

However, they point out, their study is limited by its small size and limited duration of follow-up to just 12 months. In addition 15 eyes (17%) at risk for neovascular AMD had to be excluded from the analysis because their postsurgery AMD status at 12 months could not be determined because of unavailable or ungradable images.

"Only a small percentage of study participants with AMD had definite progression to either neovascular AMD or geographic atrophy within 1 year of cataract surgery when eyes were carefully monitored with immediate preoperative and postoperative fundus photographs and fluorescein angiograms," the study authors conclude. "Our findings do not support the hypothesis that cataract surgery accelerates the progression of AMD."

In an accompanying editorial, Barbara E. K. Klein, MD, MPH, from the University of Wisconsin in Madison, writes that several reports have shown an association between cataract surgery and AMD since the late 1980s.

"Some report a cross-sectional association, some, incidence of AMD after surgery, and yet others report progression to more severe AMD. Still, there are some studies that do not find a significant association after controlling for relevant confounders. What might explain the disparate results? In my estimation, the diversity of findings in no small part begins with differences in study design," Dr. Klein noted."

Discussing these inconsistencies will help patients and their physicians make a more informed decision about the risks for progression to early AMD and development of late AMD after cataract surgery, she writes. "Until we have better information regarding the risk of developing AMD in those undergoing cataract surgery, it is the best we can do for our patients."

For more information go to www.maculardegenerationassociation.org

Obese Britain Blind to Risk of Sight Loss

2009-11-09T09:03:00.000-08:00

ANDOVER, England,

As the UK's obesity crisis burgeons, millions of overweight Brits are blind to the fact that their unhealthy lifestyles mean they are twice as likely to lose their sight as someone with a normal BMI (Body Mass Index).

A shocking new report launched by the sight charity Eyecare Trust and healthcare provider Simplyhealth to mark National Eye Week (9-15 November 2009) reveals that just eight per cent of us associate obesity with sight loss(1), despite weight being a major risk factor in the onset and progression of many sight-threatening eye conditions.

With more than half of all adults across the UK tipping the scales above their recommended weight and a staggering 23 per cent now classed as obese (2), millions of Brits are needlessly putting themselves at risk of poor vision or even worse - total sight loss.

Iain Anderson, Chairman of the Eyecare Trust warns: "Carrying excess weight causes pulmonary problems which can lead to irrevocable damage to the delicate blood vessels in the eye. A Body Mass Index of 30 or more doubles your risk of age-related macular degeneration - the UK's leading cause of blindness - and significantly increases your chances of developing cataracts or glaucoma."

The survey also found that people's perceptions about weight - and in particular obesity - are seriously wide of the mark. For example, four fifths of those polled (82 per cent) believed a man of 6ft weighing 13st 3lb is healthy, when in fact he is overweight.

Iain continues: "While people are more likely to be aware of threat to eye health from factors such as smoking, excessive alcohol consumption or poor diet, they just don't make the connection with obesity, which can also put people at risk of diabetic retinopathy whether or not they suffer from diabetes." The strong links between obesity and eye disease have been affirmed by recent international research undertaken by eminent ophthalmologists in Israel and Singapore(3).

Regular sight tests are vital for the early diagnosis and treatment of these eye conditions, yet the National Eye Week 'See the Benefit' poll found that obese people were the group least likely to visit their optician. Worryingly, the survey reveals that those with a BMI in excess of 25 are most likely to believe their eyes are in a state of 'good' or 'very good' health(4).

Raman Sankaran of Simplyhealth says: "As well as lifestyle choices having an impact on eye health, the research also worryingly found that cost - or the issue of perceived cost - affects whether people attend regular sight tests. In fact 75 per cent of people admit to putting off having their eyes tested due to the price of the examination and the expense of glasses or contact lenses if needed.

"Attending a sight test needn't be expensive or act as a barrier to good eye health as there are many options available to help people budget for eyecare, such as a cash plan from Simplyhealth," Raman adds.

The Eyecare Trust recommends that everyone should have an eye examination every two years, unless advised otherwise by an optometrist. As well as providing a valuable insight into the health of your eyes a sight test also acts as an essential general health check uncovering a number of other underlying health problems such as high cholesterol, high blood pressure, diabetes and an increased risk of stroke.

For more information go to www.maculardegenerationassociation.org

Blue light-filtering increases macular pigment, may protect against age-related vision loss

2009-10-27T21:59:00.000-07:00

Age-related macular degeneration, a major cause of vision loss, affects millions of older persons

Results of an important new study show that implantation of blue light-filtering intraocular lens (IOLs) at the time of cataract surgery increases a nutritional component of the eye, which may afford protection against the development and/or progression of age-related macular degeneration (AMD).

The study, conducted by leading ophthalmology and vision researchers from the Macular Pigment Research Group at the Waterford Institute of Technology, is published in the October 2009 issue of the high impact journal Investigative Ophthalmology & Visual Science (IOVS).1

AMD is a disease affecting the central part of the retina and is the leading cause of vision loss in the developed world.2 Implantation of lenses that do not filter blue light during cataract surgery has been shown to increase the risk for development and/or progression of AMD.3

"Blue light-filtering lenses filter and block damaging blue light from reaching the retina, which holds the potential of reducing vision loss and improving the quality of life for millions of older patients," said the study's chief investigator, John M. Nolan, Fulbright Scholar, BSc, PhD, deputy director, Macular Pigment Research Group, Waterford Institute of Technology, Waterford, Ireland. "These data represent an important first step in fully realizing the benefits of blue light-filtering in improving a nutritional component of the eye known as macular pigment. There is a strong scientific rationale supported by an ever-growing body of scientific evidence which suggests that macular pigment plays a role in reducing the onset and progression of AMD."

Dr. Nolan and fellow Macular Pigment Research Group researchers discovered an increase in macular pigment levels shortly after cataract surgery among the study patients who had blue light-filtering IOLs implanted.1

"Since prolonged exposure to blue light is harmful to the retina, increased levels of macular pigment are considered a strong surrogate marker for protection against the processes that cause age-related blindness, including AMD," says Dr. Nolan.

According to the study, the potential benefits associated with increased macular pigment resulting from the use of blue light-filtering lenses for prevention and/or decreased progression of AMD would be conferred at the time of cataract surgery and are expected to continue thereafter, over a patient's lifetime.1 This is especially meaningful in the modern era of cataract surgery, which is being performed annually in millions of older persons who live for many years after the procedure, as well as certain patient subgroups, who have had the surgery at an earlier age.2 The researchers note that further studies are needed to confirm the clinical benefit of their findings.1

About the Study

Dr. Nolan and colleagues conducted a prospective study in which 42 patients scheduled for cataract surgery were randomized to implantation with a blue light-filtering acrylic IOL or a standard acrylic IOL (control), with macular pigment optical density measured by a reliable method (heterochromatic flicker photometry), and serum concentrations of the macular carotenoids were quantified by a scientific procedure known as high performance liquid chromatography, prior to surgery and then at several post-procedural time points over a 1-year follow-up period.1

Cataract surgery in older persons, where the natural diseased lens (cataract) is replaced with a clear artificial IOL, has been associated with increased subsequent risk for macular disease,4 perhaps due to increased transmission of potentially injurious short-wavelength (blue) light to the retina.3

Therefore, lens manufacturers have incorporated a blue light-filter into IOLs to help reduce photo-oxidative retinal injury and thereby reduce the risk of new-onset AMD and/or its progression. Evidence suggests that photo-oxidative stress is important in the development of AMD.5 The likelihood of retinal damage is highest for short-wavelength light (blue light). Several parts of the eye, most importantly the lens, act as filters to block short-wavelength light from reaching the retina.4

Macular pigment is thought to protect against AMD because it absorbs short-wavelength (blue) light before it reaches photoreceptors in the retina and because of its antioxidant properties (decreases oxidative stress by quenching free radicals). Portions of the eye behind (posterior to) macular pigment are exposed to approximately six times the amount of blue light in persons having the lowest levels of macular pigment, as compared to those with the highest levels.5 Macular pigment is obtained entirely from the diet and transported to the retina via the blood. Therefore, ongoing research is being conducted to determine to what extent a person's diet may affect AMD. However, the data available to date is in support of such a notion.5

About Cataracts and AMD

As the aging population grows and becomes a larger percentage of the overall population, age-related diseases such as cataracts and AMD will become more prevalent.6

Surgical removal of cataracts – lens that have become clouded from buildup of protein – is the most frequently performed surgery in the U.S.7, with more than 6 million cataract surgeries currently performed each year in the U.S. and Europe combined.7,8 While vision is almost universally improved immediately following cataract removal, implantation of lens that does not filter harmful short wavelength (blue) light may hasten the progression of AMD,5 the leading cause of vision loss in people over the age of 60 in the U.S.9

AMD is a disease that affects part of the back of the eye called the macula, the central part of the retina. The central vision of affected individuals becomes blurry or wavy and can be eventually lost, which severely alters their quality of life.9,10 Approximately 25-30 million individuals are affected worldwide, with the number estimated to triple in the next 25 years.11

For more information go to www.maculardegenerationassociation.org

NeoVista®, Inc. Completes Enrollment in Pivotal CABERNET™ Study

2009-10-22T14:54:00.000-07:00

Neovascular AMD affects hundreds of thousands of patients globally. It is our hope that upon one-year follow-up, the data will support FDA approval in a most timely manner so that retinal surgeons, patients, and heath care systems in the US and around the world will have a cost effective option available for treating this dreadful disease in the immediate future.

NeoVista, Inc. today announced the completion of enrollment in its global 450-patient randomized controlled study of their revolutionary epimacular brachytherapy procedure for the treatment of neovascular age-related macular degeneration (AMD). The Company will now begin the mandated one-year data follow-up before submitting the final clinical module of its Pre-Market Approval (PMA) submission to the FDA.

"It's exciting to reach this long anticipated milestone in the CABERNET Study," said John N. Hendrick, President and CEO of NeoVista. "Neovascular AMD affects hundreds of thousands of patients globally. It is our hope that upon one-year follow-up, the data will support FDA approval in a most timely manner so that retinal surgeons, patients, and heath care systems in the US and around the world will have a cost effective option available for treating this dreadful disease in the immediate future."

The largest study of its kind to date, the multi-center CABERNET (CNV Secondary AMD Treated with BEta RadiatioN Epiretinal Therapy) Study assigned patients into one of two arms: a control arm where patients were administered regular Lucentis® (Genentech, South San Francisco, CA) injections and a one time surgical arm, where patients were administered a dose of strontium-90 beta radiation via a short surgical procedure, followed by concomitant injections of Lucentis when needed. The primary efficacy endpoint for the CABERNET Study is based on one-year follow-up of the surgical arm cohort when compared to the control group.

"The CABERNET Study has brought together multi-disciplinary clinical teams aligned around the mission of addressing the serious problem of neovascular AMD," said Pravin U Dugel, Managing Partner, Retinal Consultants of Arizona, Phoenix, Arizona and principal investigator for the CABERNET Study. "I look forward to the final results of this ambitious clinical trial. More than any other recent trial, this clinical trial has the potential of improving the quality of life and the overall treatment of patients with neovascular AMD. It could potentially have a significant impact on the practice patterns and economics of retinal physicians as well as global health care systems."

For more information go to www.maculardegenerationassociation.org

Signs Of Macular Degeneration May Predict Heart Disease

2009-10-13T14:33:00.000-07:00

A large study found strong evidence that older people who have age-related macular degeneration (AMD) are at increased risk for coronary heart disease (CHD), although not for stroke. This result adds to mounting evidence that AMD and cardiovascular disease may share some risk factors--smoking, high blood pressure, inflammatory indicators such as C-reactive protein, genetic variants such as complement factor H--and disease mechanisms.

For more information go to www.maculardegenerationassociation.org

Patent-pending process improves eye disease detection

2009-10-05T22:00:00.000-07:00

Memphis Business Journal - by Michael Sheffield

A collaboration between two professors at the University of Memphis and Southern College of Optometry could result in earlier detection of retinal diseases through a patent-pending testing process.

The Pseudo 2D Fractal Analysis was developed through a collaboration between Khan Iftekharuddin, associate professor in the Department of Electrical and Computer Engineering at the University of Memphis, and Pinakin Gunvant, assistant professor at Southern College of Optometry.

The process uses light beamed through the back of the retina to measure the thickness of retinal tissue at certain points. If the tissue is thick at the “12 and six o’clock” points, it is an indicator of glaucoma. The reflection of the light provides an indicator of the tissue’s thickness.

Gunvant says previous testing methods were accurate 85% of the time, but the 2D method has proven to be 98% accurate.

“That’s very clinically significant,” Gunvant says. “But you’re not inventing new devices. You’re just analyzing the data better.”

Gunvant and Iftekharuddin were doing separate research, with Gunvant focusing on retinal research at the Southern College and Iftekharuddin doing imaging work at the U of M. Gunvant said neither of the two had any idea the other existed until he looked Iftekharuddin up online. Ironically, the U of M professor was out of the country when Gunvant first contacted him.

“I found him through my good friend, Google, and he was right down the road,” Gunvant says. “If it wasn’t for technology, we might have never met.”

Iftekharuddin had used imaging to detect brain tumors through work with St. Jude Children’s Research Hospital, but hadn’t done any research with glaucoma. He says fractal imaging is able to pick up any irregularities in shapes or signals.

“We just took that and applied it to glaucoma and the results turned out to be excellent,” Iftekharuddin says. “Like any other disease, if you diagnose early you can treat it better.”

Once the two professors ensured the technique worked, the University of Memphis began the patent process, which can take up to three years. But it could also yield a viable product for the school to market and license, says Kevin Boggs, director of technology transfer and research development at the University of Memphis.

Boggs says the length of the patent process won’t prevent the two schools from marketing the product to companies that have a history of licensing patent applications.

“Once they’re familiar with the product, they’ll invest in it knowing the odds of getting a patent,” Boggs says. “There are a couple of options. We could either go with an exclusive or non-exclusive license, but we’d have to look at what would bring the product to the broadest possible market to help the most people.”

Gunvant says the technique could also detect other causes of blindness, like diabetes or macular degeneration. The immediate focus, however, is glaucoma, which is the second-leading cause of blindness in the world and the leading cause of blindness among African-Americans.

Gunvant says the new focus of the research will be trying to reach 100% accuracy.

“I doubt we’ll ever hit 100%, but most scientists get proven wrong in 15 years,” Gunvant says. “Glaucoma is very variable and affects different individuals in different ways. We’d have to do a very large scale study to get better than where we are at the moment.”

Gunvant says the technique probably would not have been perfected without the team effort.

“It’s hard to be an expert in every field, so multi-disciplined collaboration is required,” he says. “When you look at a problem from one angle, your brain gets fried, so you have to have someone else to come in and help you solve it.”

For more information go to www.maculardegenerationassociation.org

Retinal implant could help the blind see

2009-09-25T17:58:00.000-07:00

By Emma Woollacott

MIT researchers are working on a retinal implant that could help blind people regain a useful level of vision.

It's designed for sufferers of retinitis pigmentosa and age-related macular degeneration, two of the leading causes of blindness. It won't restore normal vision, but could help blind people get around more easily.

Patients would wear a pair of glasses with a camera that sends images to a microchip attached to the eyeball. The glasses contain a coil that wirelessly transmits power to receiving coils surrounding the eyeball.

When the microchip receives visual information, it activates electrodes that stimulate nerve cells in the areas of the retina corresponding to the features of the visual scene. The electrodes directly activate optical nerves that carry signals to the brain, bypassing the damaged layers of retina.

In previous implants, the electrodes were attached directly to the retina from inside the eye, which carries more risk of damage. In the latest version, the implant is attached to the outside of the eye, and the electrodes are implanted behind the retina.

The team has been working on the implant for 20 years, and hopes to start testing it in blind patients within the next three years. The goal is to produce a chip that can be implanted for at least 10 years.

They've tried it out in Yucatan miniature pigs, which have roughly the same sized eyeballs as humans, purely to determine whether the implants remain functional and safe. So far, the prototypes have been successfully implanted in pigs for up to 10 months.

The researchers hope that once human trials begin and blind patients can offer feedback on what they're seeing, they will learn much more about how to configure the algorithm implemented by the chip to produce useful vision.

Patients have said that what they would like most is the ability to recognize faces. "If they can recognize faces of people in a room, that brings them into the social environment as opposed to sitting there waiting for someone to talk to them," says Shawn Kelly, a researcher in MIT's Research Laboratory for Electronics.

For more information go to www.maculardegenerationassociation.org

High-tech glasses help the nearly blind see

2009-09-18T09:28:00.000-07:00

CBC News

An Ottawa company is developing computerized glasses that help people with severe visual impairments see — as well as zoom in on and replay what they saw with the press of a button.

The company, eSight Corp., received a $500,000 grant from the Ontario government this week to develop its evSpex product as part of a special $4.5 million fund to help 10 start-up companies bring products to market.

The device, which resembles a pair of large sunglasses, has a high-resolution camera on the outside and tiny LCD screens on the inside that project images to the wearer's eyes.

Before the image is projected, it's custom-processed by a tiny computer, said company president Rob Hilkes.

"So that when it's presented to a person who has diseased eyes … it's presented to the pieces of their vision that are most functional," he added.

Réjean Munger, a senior scientist at the Ottawa Hospital Research Institute who helped develop the glasses, said that can help people with a variety of diseases.

"We can take advantage of every bit of vision they have," he said.

The company hopes to start commercial production next year.

Sister of company chairman inspiration for glasses
Anne Lewis, who is legally blind as a result of Stargardt's disease, has been testing the prototype and is very excited about it.

"I see this product as a gift; I truly do," she said at the news conference announcing the funding.

Lewis is the sister of Conrad Lewis, eSight's chairman and one of the company's founders, and her disability was the inspiration for the glasses.

Stardgardt's disease is a form of macular degeneration that has destroyed Anne Lewis's sight except for her peripheral vision.

"It's like looking at a bubble and the inside of the bubble is black, the outside is clear," she said.

Lewis said using the glasses will allow her to read body language in meetings at work, stand on her deck and see flowers blooming, navigate shopping malls and flag down the right bus.

Unlike other products she has tried, it works even while she is moving.

The product is expected to be able to help people with age-related macular degeneration, diabetic retinopathy, glaucoma and retinitis pigmentosa.

Users can record, zoom
Because the device is essentially recording a loop of video at all times, it will include special functions that people with normal vision don't have. For example, the user can save the last 10 seconds of what they saw at the press of a button so they can have another look at something that went by too quickly. The video can also be viewed later on a DVD player or computer. In addition, they could zoom in on certain things in their field of view.

Hilkes said the features are available because the "inherent guts" of the device are a computer.

"Once you pack a lot of electronics into a system like this, then creative people start to think of all kinds of ways that you could use it," he said.

In the future, the company hopes to market the technology to people with normal vision as wearable binoculars, night vision goggles or video gaming devices.

For more information go to www.maculardegenerationassociation.org

Increase Your Omega-3s

2009-09-09T10:17:00.000-07:00

Within the polyunsaturated fat category, there are two important subclasses of fatty acids: omega-3s and omega-6s. Vegetable oils are rich in omega-6 fatty acids, and most Americans unknowingly get plenty of them in the diet. On the other hand, omega-3 fatty acids, which are found in fish and shellfish, tofu, flax, nuts and canola and soybean oils, are generally lacking in our diets.

Omega-3s appear to have a positive effect on heart rhythm and according to one recent study, may even reduce the incidence of the most common type of stroke. In fact, on the basis of the current research, the U.S. Food and Drug Administration approved the use of a qualified health claim for dietary supplements of omega-3 fatty acids relating them to a reduced risk of heart disease.

Another intriguing area of research on omega-3 fatty acids pertains to their role in brain and visual function, as some research suggests they may have a role in preventing macular degeneration, a common form of blindness.

Continuing research involves the role of omega-3 fatty acids and the immune system, and suggests a positive influence on rheumatoid arthritis, asthma, lupus, kidney disease and cancer, as well as promising research at the National Institutes of Health on depression.

For more information go to: www.maculardegenerationassociation.org

Palladium-103 plaque radiation therapy for macular degeneration: results of a 7 year study

2009-09-02T18:56:00.001-07:00

Aim: To report 7 year results of ophthalmic plaque radiotherapy for exudative macular degeneration.

Methods: In a phase I clinical trial, 30 patients (31 eyes) were treated with ophthalmic plaque irradiation for subfoveal exudative macular degeneration. Radiation was delivered to a mean 2 mm from the inner sclera (range 1.2–2.4) prescription point calculated along the central axis of the plaque. The mean prescription dose was 17.62 Gy (range 12.5–24) delivered over 34 hours (range 18–65). Early Treatment Diabetic Retinopathy Study (ETDRS) type standardised visual acuity determinations, ophthalmic examinations, and angiography were performed before and after treatment. Clinical evaluations were performed in a non-randomised and unmasked fashion.

Results: At 33.3 months (range 3–4), 17 of 31 (55%) eyes had lost 3 or more lines of vision on the ETDRS chart, five (16%) had improved 3 or more lines, and the remaining nine (29%) were within 2 lines of their pretreatment visual acuity measurement. Overall, 45% of patients were within or improved more than 2 lines of their initial visual acuity. Five eyes developed macular scars, eight developed subsequent neovascularisation or haemorrhage, and three progressed through therapy. Two patients were lost to follow up. The most common finding of patients followed for 6 or more months (n = 18 of 29 (62%)) was regression or stabilisation of the exudative process. No radiation retinopathy, optic neuropathy, or cataracts could be attributed to irradiation.

Conclusion: Ophthalmic plaque radiation can be used to treat exudative macular degeneration. At the dose and dose rates employed, most patients experienced decreased exudation or stabilisation of their maculas. No sight limiting radiation complications were noted during 7 year follow up. Owing to the variable natural course of this disease, a prospective randomised clinical trial should be performed to evaluate the efficacy of plaque radiation therapy for exudative macular degeneration.

Researchers Grow Eye Cells From Skin Cells

2009-08-28T12:27:00.000-07:00

Researchers have succeeded in growing light-sensing eye cells from human skin cells, opening the possibility of restoring sight to patients blinded by certain diseases.

Researchers at the University of Wisconsin have grown retinal cells from skin cells, a development that could be used to treat degenerative eye diseases.

A number of genetic disorders involve the degeneration of the retina, the light-sensitive cells at the back of the eye. The disorders cause the cells to die, and vision is gradually lost, resulting in blindness.

The researchers manipulated human skin cells to act like embryonic stem cells, which can be coaxed to grow into any tissue in the body. The development suggests that doctors may someday be able to repair damage to the retina with new cells generated from the patient's own skin.

Lead researcher David Gamm, a professor of ophthalmology and visual sciences at the University of Wisconsin, says his research could benefit people with macular degeneration and retinitis pigmentosa. In both diseases, the visual field gradually narrows, eventually leading to blindness.

"In particular these diseases are quite devastating to the patients who are affected by them," he said. "They rob them of their vision either when they are younger in the case of retinitis pigmentosa or when they are older in the case when they are older in the case of macular degeneration. And there are no cures and very few if any treatments for them. So it is a big need, especially from the macular degeneration standpoint, as the population ages."

An estimated one million people worldwide are affected by macular degeneration alone.

Gamm says the laboratory process of creating human retinal cells helps researchers better understand how eyes develop, so diseases that lead to vision loss may someday be treated or even cured with retinal stem cells.

The development could also further research on genetic eye conditions. For example, using skin cells from a patient with retinitis pigmintosa researchers could create retinal cells with the defective gene and subject them to various potential drugs for treating or curing the condition.

Gamm says the same technique could help scientists find treatments for other genetic diseases, not just eye disorders.

"Now we could take theoretically any human disease, especially those that have specific gene defects underlying them, and produce cell types of interest in those diseases and test them directly for the efficacy of various drugs or how in fact those cells die in disease," he added.

The study on the development of eye cells is published this week in the journal Proceedings of the National Academy of Sciences.

By Jessica Berman
Washington

An Overview of Macular Degeneration Research

2009-08-04T13:09:00.000-07:00

Doctors and scientists are currently conducting macular degeneration research. Macular degeneration research studies are designed to answer important questions and to find out whether new approaches are safe and effective. This research already has led to many advances, and researchers continue to search for more effective methods for dealing with macular degeneration.

Current Areas of Focus in Macular Degeneration Research
A number of macular degeneration research studies are being conducted to learn what causes macular degeneration and how it can be better treated.

One macular degeneration research study is also evaluating the effects of certain vitamins and minerals in preventing or slowing the progress of the disease.

At the same time, scientists studying macular degeneration are trying to learn more about how the cells in the retina work. This knowledge will allow them one day to pinpoint the causes of macular degeneration and come up with ways to prevent it.

Other areas of current research include:

* Studying the possibility of transplanting healthy cells into a diseased retina
* Evaluating families with a history of macular degeneration to understand genetic and hereditary factors that may cause the disease
* Looking at certain anti-inflammatory treatments for the wet form of macular degeneration.

This macular degeneration research should provide better ways to detect, treat, and prevent vision loss in people with the disease.

for more information www.maculardegenerationassociation.org

Novel Biomarker for Age-Related Macular Degeneration

2009-07-12T19:24:00.000-07:00

A team of researchers at the University of Kentucky has discovered a biological marker for neovascular age-related macular degeneration (AMD), the leading cause of blindness in older adults. The scientists say the biomarker shows strong potential as a means for both the early detection of the disease and for preventive treatment.

The Aging Eye: Researchers Aim To Stop the Clock

2009-06-06T15:50:00.000-07:00

By JANE E. BRODY

AGING Americans expect more from their eyes these days than ever before. People in their 70's and 80's want to be able to drive, play cards, recognize people on the street, travel with their grandchildren, take advantage of senior discounts in the movies and read the books they missed while working full time.

But eyes have a way of aging that can render such expectations unrealistic. Far worse than the loss of visual acuity that prompts most middle-aged people to resort to magnifying lenses are sight-robbing diseases like glaucoma, cataracts, age-related macular degeneration, diabetic retinopathy and other retinal disorders that afflict tens of millions of Americans, usually after age 50.

The incidence of such potentially blinding disorders is increasing rapidly as the number of older people grows. Experts predict, for example, that by the year 2030, 6.3 million older Americans will develop macular degeneration, up from 1.7 million in 1995. It is a still-irreversible disorder that robs people of the central vision needed to drive, read, watch television, recognize faces, play cards or do any fine work. If Grandma Moses had had macular degeneration, her artistic talents would never have been noticed.

Fortunately, research is progressing on a number of promising new treatments, including low doses of radiation, and a combination of lasers and light-activated chemicals, both of which are used for some particularly hard-to-treat forms of macular degeneration. Other research is concentrating on how to stop toxins that damage the eye in glaucoma, and the genetics of several different eye diseases.

''Older Americans today expect to enjoy their retirement with the same visual capacity that they had in their younger years,'' said Dr. Harold Spalter, professor of ophthalmology at Columbia-Presbyterian Medical Center in New York. But, alas, as was apparent at a four-day seminar that Dr. Spalter chaired here last month, researchers are still a long way from knowing how to reverse most blinding eye disorders.

Still, major progress in understanding and treating these conditions -- and perhaps detecting them early enough to blunt their effects -- was evident at the seminar, organized by Research to Prevent Blindness, a New York-based voluntary organization. Unfortunately, though, many elderly Americans cannot afford the early detection procedures described at the seminar because Medicare and many other insurance programs do not cover such preventive measures.

For example, while insurance companies would routinely cover a visual field examination for a patient who already has glaucoma, most would not pay for this test for a person who has not yet experienced vision loss, when the disease process might be stopped without lasting vision damage.

Furthermore, an ongoing study of 2,520 men and women aged 65 to 84 in Salisbury, Md., has revealed that the usual eye chart test for visual acuity is inadequate to assess vision losses that interfere with the ability of elderly people to get around on their own, perform tasks of daily living and avoid accidents that can result in serious or fatal injuries. Rather, Dr. Sheila West, professor of ophthalmology at Johns Hopkins Medical Institutions, reported that tests for contrast sensitivity -- the ability to distinguish, say, a step from the one below it -- are more revealing of functional disability in older people.

''We have found that loss of contrast sensitivity is as important as arthritis and heart failure in determining loss of mobility in the aged,'' Dr. West said. She traced this loss to ''nonspecific retinal changes'' and the beginnings of cataracts, a gradual clouding of the lens of the eye that eventually obscures vision. However, early-stage cataracts are rarely recognized by those who have them and are often dismissed as inconsequential by eye doctors.

Sunlight, Dr. West said, is a major factor in the formation of cataracts, and the damage is cumulative. By assessing the exposure of study participants to sunlight, Dr. West and colleagues determined that for every 1 percent increase in exposure to ultraviolet-B light, the risk of developing cataracts rose by 10 percent.

''There is no threshold for sun-related damage, the dosage is cumulative and no group is immune to it,'' Dr. West said the study showed. She recommended that when out of doors, everyone -- starting in childhood -- should wear lenses that block ultraviolet light and a cap with a brim that shades the eyes.

Dr. M. Cristina Leske, head of preventive medicine at University Medical Center in Stony Brook, N.Y., and associates, identified other risk factors for cataracts. Through a five-year study of 764 patients, they found that Caucasians are three times as likely as blacks to develop cataracts. Those who take the gout medicine allopurinol face more than a two-fold increase in risk, and smokers have a 60 percent increase.

On the other hand, certain nutrients appear protective. The risk was 30 percent lower among those who took multivitamin-mineral supplements and nearly 60 percent lower among those who took a vitamin E supplement, a finding that is now being tested in a clinical trial sponsored by the National Eye Institute. Still another study of 247 women aged 56 to 71 conducted at Tufts University in Boston found that taking vitamin C supplements for more than 10 years reduced the risk of early cataracts by 77 percent and the risk of moderately advanced cataracts by 83 percent.

But while cataracts can usually be treated very successfully by surgically removing the damaged lens and replacing it with a synthetic lens implant, age-related macular degeneration, the leading cause of legal blindness in the elderly, has yet to yield to an effective treatment. Macular degeneration involves progressive damage to the cells in the center of the retina that are responsible for straight-ahead vision.

Early cases are often treated with lasers, which have the unfortunate side effect of destroying normal retinal cells as well as the damaged areas beneath them. Furthermore, after laser treatment, the vision-damaging tissue often grows back.

Dr. Dennis M. Marcus, an ophthalmologist at the Medical College of Georgia in Augusta, said that laser therapy usually cannot be used for the most severe form of the disease -- so-called wet macular degeneration, which involves the growth of leaky blood vessels beneath the central retina. Instead, he and his colleagues are testing low-dose radiation to destroy the blood vessels but spare the normal retinal cells. Thus far, 100 patients have been treated in a clinical trial that will eventually involve 500 people with wet macular degeneration. While it is too soon to evaluate the effectiveness of the treatment, Dr. Marcus said that he has seen no radiation-induced complications.

Another clinical study is testing a technique called photodynamic therapy. It starts with the intravenous administration of a photosensitive dye that collects in the damaging blood vessels that are growing beneath the retina. The eye is then exposed to laser light that activates the dye, destroying those vessels only. Dr. Joan W. Miller, an ophthalmologist at the Massachusetts Eye and Ear Infirmary, said that preliminary studies showed that the technique effectively closes off the leaky vessels in the majority of patients. And while these vessels reopen and leak in some patients, the treatment can be repeated, if needed, without harm to the eye.

Some seminar participants said the best hope for conquering blinding eye diseases was unraveling the sometimes complex genetics underlying many if not all of these conditions. Just last month, for example, a team of scientists announced the discovery of the first genetic link to age-related macular degeneration, which strikes 25 percent of Americans over the age of 65 and is the major cause of vision loss in the elderly. The researchers hope that by studying mutations in this gene they will gain an understanding of how the disease damages the eye, a means of identifying those at risk and methods of prevention and treatment.

Glaucoma, for example, usually involves elevated pressure inside the eye, leading eventually to the death of ganglion cells, the nerve cells that transmit information from the eye to the brain. This disease afflicts perhaps eight million Americans and causes blindness in 5,500 each year. Currently the only available treatment involves continual use of eye drops that reduce intraocular pressure. This only works if treatment is begun early.

Dr. Robert W. Nickells, an eye researcher at the University of Wisconsin in Madison, said, however, that ''new advances suggest that glaucoma could be treated during the second or even the third stage of the disease.'' The second stage involves the release of high concentrations of ''excitotoxins,'' amino acids that are toxic to nerve cells. Dr. Nickells said that several compounds that intervene in the formation of excitotoxins have been developed to treat other neurodegenerative disorders and may also prove useful in treating glaucoma.

As for the third stage, he and his colleagues have found in monkeys and rodents that ganglion cells succumb to a form of programmed cell death that appears to be controlled by three genes that act as a molecular switch. One of the genes, called bcl-x, prevents the fatal blow and might be harnessed therapeutically to override the cell death mechanism, Dr. Nickells said.

But discoveries about the genetics of eye disorders can sometimes raise more questions than they answer. For example, Dr. Fulton Wong of Duke University Medical Center reported that as many as 50 genes are believed to be involved in the progressive disease retinitis pigmentosa, which begins as night blindness and loss of peripheral vision and eventually destroys central vision, leaving people blind. Thus far, four genes have been identified, each with multiple mutations that may result in different aberrations of the condition. One of the genes that codes for the production of the visual pigment rhodopsin can exist in 92 different mutated forms, Dr. Wong reported.

This year alone, three genes for various forms of glaucoma have been identified. But Dr. Janey Wiggs, an ophthalmologist and geneticist at Tufts University School of Medicine in Boston, said: ''This is a very complicated disease, with maybe 20 or 30 genes involved. And finding genes is only the first step. Where and when is the gene required and how does it produce disease? Does it result in too much or not enough of a gene product or make a toxic product?''

Still, she and others expressed guarded enthusiasm for the prospects of gene therapy to treat various devastating eye diseases. ''The eye is accessible,'' she said. ''It can be given selective treatment, using the other untreated eye as a control to see how well the treatment is working.''

Dr. J. Timothy Stout, head of the division of ophthalmology at Children's Hospital in Los Angeles, said, ''The potential use of gene therapy is nearly limitless for the ophthalmologist.'' He and his colleagues are exploring in animals the potential of a so-called suicide gene to treat eye diseases that involve excessive cell division, such as intraocular proliferative disease, macular degeneration and diabetic retinopathy. Normally, most cells in an adult eye are not dividing. Using as a gene carrier a virus that infects only actively dividing cells, he introduces into the eye a gene that by itself is not toxic but that results in cell death when combined with the drug ganciclovir, which also does not harm normal cells. Thus, the treatment is specific for the proliferating cells involved in the eye disease.

New uses for existing drugs

2009-05-30T20:41:00.000-07:00

REPRINTED FROM THE NEW YORK TIMES

Housed in a row of white freezers in a nondescript laboratory at the Johns Hopkins University School of Medicine in Baltimore are more than 3,000 of the estimated 10,000 drugs known to medicine. There is no sign on the door to indicate that this is perhaps the largest public drug library available to researchers interested in finding new uses for old and often forgotten drugs.

Already, researchers have used the library to discover that itraconazole, a drug used for decades to treat toenail fungus, may also inhibit the growth of some kinds of tumors and may forestall macular degeneration. Another drug, clofazimine, used more than a century ago to treat leprosy, may be effective against autoimmune disorders like multiple sclerosis and psoriasis.

“It takes 15 years and costs close to a billion dollars to develop a new drug,” said Jun O. Liu, professor of pharmacology and director of the Johns Hopkins Drug Library. “Why not start with compounds that already have proven safety and efficacy?”

He and his colleagues have been building the collection since 2002 and hope to have it complete by 2011. They acquire the drugs through donations, purchases and sometimes lab synthesis. And they will send researchers a complete set — minuscule amounts of every drug in the library — for $5,000, which covers the cost of shipping and replenishment.

Since the toenail and leprosy drugs are approved for use in the United States and are no longer under patent protection, clinical trials to test their new uses are either under way or close to regulatory approval, Dr. Liu said.

Drugs still under patent protection are more complicated; patent holders seldom allow independent research on alternative uses. “The drug companies haven’t been too keen on helping us,” Dr. Liu said.

There are other drug libraries, both commercial and noncommercial. Commercial suppliers offer considerably fewer drugs than Johns Hopkins (though they may have medicines it does not), and they charge much more. Noncommercial drug libraries include those at the National Institutes of Health; the University of California, San Francisco; and McMaster University in Hamilton, Ontario. But they will usually not send drugs to unaffiliated researchers. And like the commercial libraries, their holdings are smaller and composed largely of compounds from Hopkins.

Regardless of the source, researchers typically order copies of entire collections rather than individual drugs they think may work in their experiments.

“We’ve found drugs that are active in ways no one would have ever hypothesized,” said Marc G. Caron, a professor of cell biology at Duke who is using the Johns Hopkins library to find drugs that might quell the cravings of substance abusers.

Testing of these compounds has become much easier in recent years as a result of an automated technology called H.T.S., for high-throughput screening. The drugs are dissolved in a solution and stored in rectangular, compartmented plates reminiscent of ice trays; they can then be delivered to researchers for testing of their efficacy against various diseases, or disease mechanisms like inflammation.

Computerized droppers, plate agitators and microscope image readers can now accomplish in days what it once took bench scientists years to do.

Although H.T.S. has been around for at least a decade, it is just within the last five years that the technology has been widely available. Previously, only big pharmaceutical companies could afford to screen thousands of compounds; now more public and academic institutions are doing so, and their emphasis tends to be on rediscovering or tweaking the chemical structure of old drugs rather than developing new ones.

“The instrumentation to do sophisticated, large-scale screening of drugs has gotten significantly better and cheaper,” said Michelle Arkin, associate director of the Small Molecule Discovery Center at U.C. San Francisco.

Some institutions, like McMaster in Ontario and Rockefeller University in New York City, allow outside researchers to use their H.T.S. facilities for $10,000 to $20,000, depending on the complexity of the project.

Access to such facilities has increased demand for compounds, particularly already approved and off-patent drugs, to analyze. Johns Hopkins and commercial suppliers report a surge in orders over the last two years — because there are more H.T.S. laboratories, they said, and because of efforts to find cheaper therapies against third world scourges like malaria and tuberculosis.

“Old drugs are the low hanging fruit in terms of finding safe and inexpensive treatments for these diseases,” said Carl Nathan, chairman of microbiology at Weill Cornell Medical College in New York. Dr. Nathan receives plates of drugs from Johns Hopkins as well as commercial suppliers and does high-throughput screening at Rockefeller, which has a partnership with Weill.

“I’m addicted to it,” he said.

Researchers aim for rare treatment of macular degeneration

2009-05-10T10:05:00.000-07:00

Friday, May 1, 2009
Researchers aim for rare treatment of macular degeneration
By Marc Songini

One of the most prevalent eye diseases is age-related macular degeneration, affecting millions in the United States, and there are few if any cures, or even approved treatments, say experts. That makes the work of a group of local researchers developing an implanted treatment particularly vital.

The AMD ailment takes two forms: One is “wet” and involves blood vessels and has limited treatments, including Lucentis, a drug from San Francisco-based Genentech Inc. (now part of Swiss firm Roche). The other is “dry” and occurs when light-sensitive cells malfunction. An estimated 15 million Americans have AMD.

For the 10 percent to 20 percent of AMD patients that have the wet form, the treatments are “reasonably effective,” said Paul Ashton, president and CEO of Watertown-based pSivida Corp., which develops eye treatments. “We have nothing for the 80 percent to 90 percent who have the dry form.” In part, this is because big pharma didn’t realize the huge market for eye treatments until about a decade ago, he said. Additionally, “Getting drugs into the eye without getting very high levels of drug everywhere else is very hard,” noted Ashton.

For dry AMD, in particular, there’s “a huge unmet need and a huge market,” said Emmett Cunningham, a partner with Cambridge-based Clarus Ventures LLC, a life sciences investment company. In part, said Cunningham, a doctor and eye expert based in Clarus’ South San Francisco office, this is because dry AMD is “complex,” and there is no one easily discerned cause. Also, there are no reliable animal models for testing.

“You’d have to take a big bet to get human proof of concept data,” he said. A venture capital firm would be prone to waiting till a dry AMD startup was in the Phase 2 or Phase 3 stage before investing the $20 million to move toward full approval.

However, one research team based at Boston College and the University of Massachusetts Medical School in Worcester is trying to solve the problems of AMD and other eye diseases by creating nano-structured retinal implants. These are tiny devices placed in the eye to take the place of the malfunctioning rods and cones in the retina, explained Michael Naughton, a professor of physics at BC, whose team is working on the nanotechnology of the implant.

“The implant is designed to reconnect to the surviving cell circuitry and provide the electronic stimulus formerly provided by the rods and cones,” said Naughton. Ideally, these implants could have a form factor similar to contact lenses. They would be widely available, although requiring retinal surgery. “Until such a time as genetic engineering can cure or regenerate rods and cones, these artificial retinas could provide a viable path to restoring vision.” Potentially, the market is worth hundreds of millions of dollars annually, he estimated.

Currently, he estimates that he needs $42 million to pay for the prototype and the animal and human studies over the next 18 months. He said there are no implants on the market for consumer use at this time, though a number are in development.

Cunningham noted that for an investor, implants are an interesting area, but the key is getting compelling data that the technical risks associated with the device have been met, because it requires surgical implantation. Also, a startup must demonstrate the size of the market is big enough related to the cost of the device, he said.

Other firms working to treat AMD and other eye ailments include Lincoln, R.I.-based Neurotech Pharmaceuticals Inc., whose lead candidate NT-501 is an intraocular implant made of genetically modified human cells. In March, it released Phase 2 exploratory study data that indicated positive results in AMD treatment, with no “serious adverse events,” said Ted Danse, president and CEO of Neurotech.

Also, pSivida’s drug Iluvien is in Phase 2 trials for both forms of AMD, said Ashton. And New Haven, Conn.-based Optherion Inc. is developing a diagnostic service and drug platform for AMD. By year’s end, Optherion plans to file an independent new drug application (IND) submission to the U.S. Food and Drug Administration for its drug, said Colin Foster, CEO and president.

For the past several years, Bedford-based Resolvyx Pharmaceuticals Inc. has been evaluating its Resolvin inflammation control drug’s effectiveness against AMD, as well.

Functional annotation of the human retinal pigment epithelium transcriptome

2009-05-03T02:03:00.000-07:00

Functional annotation of the human retinal pigment epithelium transcriptome

To determine level, variability and functional annotation of gene expression of the human retinal pigment epithelium (RPE), the key tissue involved in retinal diseases like age-related macular degeneration and retinitis pigmentosa. Macular RPE cells from six selected healthy human donor eyes (aged 63-78 years) were laser dissected and used for 22K microarray studies (Agilent technologies).

Data were analyzed with Rosetta Resolver, the web tool DAVID and Ingenuity software.

Results: In total, we identified 19,746 array entries with significant expression in the RPE. Gene expression was analyzed according to expression levels, interindividual variability and functionality.

A group of highly (n=2,194) expressed RPE genes showed an overrepresentation of genes of the oxidative phosphorylation, ATP synthesis and ribosome pathways. In the group of moderately expressed genes (n=8,776) genes of the phosphatidylinositol signaling system and aminosugars metabolism were overrepresented.

As expected, the top 10 percent (n=2,194) of genes with the highest interindividual differences in expression showed functional overrepresentation of the complement cascade, essential in inflammation in age-related macular degeneration, and other signaling pathways. Surprisingly, this same category also includes the genes involved in Bruch's membrane (BM) composition.

Among the top 10 percent of genes with low interindividual differences, there was an overrepresentation of genes involved in local glycosaminoglycan turnover.

Conclusions: Our study expands current knowledge of the RPE transcriptome by assigning new genes, and adding data about expression level and interindividual variation.

Functional annotation suggests that the RPE has high levels of protein synthesis, strong energy demands, and is exposed to high levels of oxidative stress and a variable degree of inflammation. Our data sheds new light on the molecular composition of BM, adjacent to the RPE, and is useful for candidate retinal disease gene identification or gene dose-dependent therapeutic studies.

Author: Judith C Booij, Simone van Soest, Sigrid MA Swagemakers, Anke HW Essing, Annemieke JMH Verkerk, Peter J van der Spek, Theo GMF Gorgels and Arthur AB Bergen
Credits/Source: BMC Genomics 2009, 10:164

National study is looking for Dry Macular Degeneration (AMD)patients for Landfall Eye Associates clinical trial

2009-04-26T03:52:00.001-07:00

National study is looking for Dry Macular Degeneration (AMD)patients for Landfall Eye Associates clinical trial

April 16th, 2009

AMD patients who are interested to volunteer the Landfall Eye Associates study, will be reimbursed to cover study related transportation costs. Approximately four visits will be required of all participants.

It's a clinical study to determine if repetitive stimulation of the preferred retinal locus, the area near the central blind spot used to focus on words, letter, and object, will help in their ability to read.

The patients will be divided into two groups. One group of patients will use a medical device that looks like a computer screen and will display bright objects to stimulate the preferred retinal locus.

Participants must be able to perform the therapy twice daily for about 40 to 50 minutes each day, six times per week. The therapy will be performed in the participant’s home for approximately three months.

The other group is the control group, will not use the medical device or perform therapy. Participants will be randomly assigned to a group.

If the trial study shows the treatment with the medical device is effective, the participants who did not perform the therapy will be offered the opportunity to do so at a later date at no charge.

Source: WebWire

Landfall Eye Associates is participating in this multicenter national study sponsored by NovaVison, Inc., headquartered in Boca Raton, Fla.

Othera reports positive interim results from Phase II dry AMD trial

2009-04-19T04:55:00.000-07:00

Othera reports positive interim results from Phase II dry AMD trial

Published:13-April-2009

By Datamonitor staff writer

137 patients enrolled at 20 leading retinal disease treatment centers across the US

Othera Pharmaceuticals, a specialty pharmaceutical company, has reported positive interim data from its Phase II trial of OT-551 in treating geographic atrophy, an advanced form of dry age-related macular degeneration for which there is no FDA-approved treatment.

According to Othera, the 12-month findings from the two-year Omega trial suggest an emerging trend for reducing moderate vision loss in patients with geographic atrophy (GA) who were treated with OT-551 compared with placebo. This numeric trend was more pronounced in subgroups based on GA characteristics or level of visual acuity at baseline.

The Omega study is a randomized, double-masked, dose-ranging, multi-center, Phase II study of topical OT-551 in patients with GA associated with age-related macular degeneration (AMD). Approximately 137 patients were enrolled at 20 leading retinal disease treatment centers across the US in this two-year study.

OT-551 has demonstrated a dose-dependent protective effect on photoreceptor activity in an animal model of AMD, and has been shown to reach the back of the eye after topical dosing in multiple species. This profile supports the rationale for studying the drug in patients with degenerative retinal conditions, such as GA, the company said.

Al Reaves, senior vice president of clinical development at Othera, said: "Based on these preliminary results, OT-551 continues to exhibit the excellent safety profile seen in prior studies. Given OT-551's safety profile and the positive trend on visual acuity, continued follow-up of this elderly population with GA should allow us to profile the drug's effect on visual acuity and better understand its long term safety."

2009-04-11T03:41:00.001-07:00

*

Feds Give Life to New Research
UCSB To Take Advantage of New Stem Cell Policy

By Sara-Fay Katz / Staff Writer

Published Wednesday, April 8, 2009

Issue 100 / Volume 89

After eight years in the cold, stem cell research is poised to benefit from the open support of the Obama administration.

Under the Bush presidency, federal funding was distributed only to researchers experimenting on 21 existing stem cell lines, thus limiting developments in the field. When President Barack Obama lifted the ban on March 9, he made federal funding available for the study of new embryonic stem lines, and UCSB researchers stand to gain from his decision.

Dennis Clegg, chair of the Dept. of Molecular, Cellular and Developmental Biology, said the Bush-era ban had significantly hindered the progress of biological research for almost a decade.

“Back in 2001, President Bush said you could only use federal funding when using existing [stem cell] lines,” Clegg said. “So, it really slowed down the progress of stem cell research in the country. Now with the lifting of the ban, it will lessen the red tape associated with this kind of study and provide new funding for stem cell research.”

Clegg said new research into regenerative medicines such as stem cells has the potential to render many fatal diseases harmless, or at least make them readily treatable.

“We are in a very exciting time for stem cell research right now,” Clegg said. “Stem cell research has great potential for treating a variety of human diseases like macular degeneration, diabetes, Parkinson’s and Alzheimer’s.”

A co-director of strategy, planning and operations at the UCSB Center for Stem Cell Biology and Engineering, Clegg said UCSB has the power to make major advancements in the growing field.

“We have quite a bit of exciting work going on in basic molecular biology and bioengineering, and we’re partnering with other universities and institutions to bring our findings to clinical applications,” Clegg said. “I think UCSB has unique strengths that will allow us to make a significant contribution in the field of stem cell research.”

Lincoln Johnson, associate director of the Center for the Study of Macular Degeneration, said the removal of the ban now ensures more options for the treatment of human diseases using natural mechanisms.

“Not all embryonic stem cell lines are the same,” Johnson said. “So for instance, with cardiac muscle for the treatment heart disease, one stem cell line might be better than another, so it’s important to have a variety. For regenerative medicine such as constructing organs, having a wider variety of stem cells to choose from will help better match the donor organ to the recipient.”

Despite the avenues of stem cell research opened by the Obama administration, Johnson said the field is still in its infancy.

“There’s a lot of research to be done, but having more cell lines and more funding will speed up the process,” Johnson said. “The better the research and the more people involved, the greater influence UCSB might have on policy formation.”

In addition to getting the go-ahead for more stem cell research, professor of chemical engineering Frank Doyle said UCSB has plans to open a new bioengineering building that will be suited for new developments in national research.

“We are in the planning stages of trying to set up a bioengineering building and we’re probably about four years away from realizing this dream,” Doyle said. “It would be a home to a rich range of engineers, chemists, biologists and physicists. I think what were hoping this building will be home to a big thrust of research on the campus, particularly an interface between medicine and engineering.”

For those interested in learning more about stem cell research, UCSB offers a class this quarter in Life Sciences Building 1001 - MCDB 146: Stem Cell Biology in Health and Disease taught by Professor Clegg. Students can also consult the UCSB Center for Stem Cell Biology and Engineering’s Web site, www.stemcell.ucsb.edu.

Brain Adapts to Age-Related Eye Disease

2009-04-05T06:24:00.000-07:00

Brain Adapts to Age-Related Eye Disease
Neurons seek input from undamaged areas to compensate, study finds

(HealthDay News) -- When macular degeneration causes one to start losing his or her sight, the affected neurons simply start seeking visual input from other, non-affected parts of the eye, Massachusetts Institute of Technology researchers report.

"This study shows us one way that the brain changes when its inputs change. Neurons seem to want to receive input: When their usual input disappears, they start responding to the next best thing," senior author Nancy Kanwisher, of MIT's McGovern Institute for Brain Research, said in an university news release.

The researchers found when the cells in the fovea, the part of the retina responsible for the central field of vision, were damaged by macular degeneration (MD) -- the neuron attached to them begin responding to stimuli in an undamaged section -- a type of internal reorganization of the eye's visual map as opposed to the cortex's work being shifting to other neurons.

"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information-processing strategy," Kanwisher said.

The findings are published in the March 4 issue of the Journal of Neuroscience.

Macular degeneration, the most common form of adult blindness, affects almost 2 million people in the United States. Patients often compensate for lack of central vision by rolling their eyes upward so they can utilize the preferred retinal locus (PRL), an undamaged area under and adjacent to the affected part of the retina.

"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said.

MD Linked with Range of Illnesses

2009-03-30T04:36:00.001-07:00

TUESDAY, Mar. 10 (HealthDay News) -- Elderly patients with age-related macular degeneration are more likely than their counterparts without the eye disease to experience a wide range of illnesses, including depression, hip fracture and blindness, according to a report published in the March issue of the Archives of Ophthalmology.

Ashley Wysong, of Duke University School of Medicine in Durham N.C., and colleagues studied Medicare claims data on 32,702 adults aged 68 years and older who were newly diagnosed with age-related macular degeneration in 1994 and 32,702 matched controls, who were all followed up in 2004 to ascertain the prevalence of a range of health conditions.

Rates of blindness, vision loss, depression, hip fracture and nursing home residence were higher among the patients with age-related macular degeneration versus those without, and they had a higher prevalence of 11 other general health conditions such as congestive heart failure, dementia and liver disease, the investigators found.

"This nationally longitudinal study documents increased rates of visual and functional health complications that occurred within 10 years of an age-related macular degeneration diagnosis," the authors write. "These findings demonstrate that the health issues of the age-related macular degeneration population are multifaceted, especially when viewed in a 10-year period, highlighting the importance of a multidisciplinary, integrated approach to the care of elderly persons with an age-related macular degeneration diagnosis."

New Technique May Spot Evidence of Macular Degeneration Years Earlier

2009-03-21T07:40:00.001-07:00

New Technique May Spot Evidence of Macular Degeneration Years Earlier

February 26, 2009

Adapted from Rochester University

A layer of "dark cells" in the retina that is responsible for maintaining the health of the light-sensing cells in our eyes has been imaged in a living retina for the first time.

The ability to see this nearly invisible layer could help doctors identify the onset of many diseases of the eye long before a patient notices symptoms. The findings are reported in the February, 2009 issue of Investigative Ophthalmology and Visual Science.

"Our goal is to figure out why macular degeneration, one of the most prevalent eye diseases, actually happens," says David Williams, director of the Center for Visual Science and professor in the Institute of Optics at the University of Rochester. "Macular degeneration affects one in 10 people over the age of 65, and as the average age of the U.S. population continues to increase, it is only going to get more and more common. We know these dark retinal cells are compromised by macular degeneration, and now that we can image them in the living eye, we might be able to detect the disease at a much earlier stage."

In 1997, Williams' team was the first to image individual photoreceptor cells in the living eye, using a technique called adaptive optics, which was borrowed from astronomers trying to get clearer images of stars. To image the dark cells behind the photoreceptors, however, Williams employed adaptive optics with a new method to make the dark cells glow brightly enough to be detected.

The cells, called retinal pigment epithelial, or RPE cells, are nearly black, and form a layer that recharges the photoreceptor cells of the eye after they are exposed to light, Williams explains. The photoreceptors contain molecules called photopigments. When light strikes these molecules, they absorb the light and change shape, sending a signal to the brain indicating they've "seen" light.

Once a photopigment molecule absorbs light, says Williams, it needs to get recharged, so it is shuttled out of the photoreceptor and down to the RPE cells. The RPE cells recharge the photopigment molecules and send them back to the photoreceptors to start the process again. In addition, the RPE layer keeps the photoreceptors healthy by collecting and storing toxic waste products that are produced during the process of regenerating the photopigment. In macular degeneration, for reasons that are not yet completely clear, the RPE cells are unable to provide this support for the photoreceptors and both kinds of cells eventually die.

Given their critical role supporting the photoreceptors, Williams says that scientists will benefit from being able to image RPE cells in patients to see what is malfunctioning in individual cells.

Williams and his team now hope to learn exactly how RPE cells are related to macular degeneration. At the moment, scientists aren't sure how the disease starts, but being able to monitor the health of individual RPE cells may help doctors begin to piece together a picture of what mechanisms are malfunctioning in the retina. Williams also says that since the technique may eventually be able to spot illness in the RPE long before the patient experiences symptoms, doctors could start patients on therapies early enough to possibly slow or stop the onset of macular degeneration. Currently, when a patient begins treatment, a great deal of irreparable damage has been done.

What Drives Brain Changes in Macular Degeneration

2009-03-14T05:48:00.000-07:00

ScienceDaily (Mar. 13, 2009) — In macular degeneration, the most common form of adult blindness, patients progressively lose vision in the center of their visual field, thereby depriving the corresponding part of the visual cortex of input. Previously, researchers discovered that the deprived neurons begin responding to visual input from another spot on the retina — evidence of plasticity in the adult cortex.

Just how such plasticity occurred was unknown, but a new MIT study sheds light on the underlying neural mechanism.
"This study shows us one way that the brain changes when its inputs change. Neurons seem to 'want' to receive input: when their usual input disappears, they start responding to the next best thing," said Nancy Kanwisher of the McGovern Institute for Brain Research at MIT and senior author of the study appearing in the March 4 issue of the Journal of Neuroscience.
"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information processing strategy," said Kanwisher, the Ellen Swallow Richards Professor of Cognitive Neuroscience in MIT's Department of Brain and Cognitive Sciences.
Macular degeneration affects 1.75 million people in the United States alone. Loss of vision begins in the fovea of the retina — the central area providing high acuity vision that we use for reading and other visually demanding tasks. Patients typically compensate by using an adjacent patch of undamaged retina. This "preferred retinal locus" (PRL) is often below the blind region in the visual field, leading patients to roll their eyes upward to look at someone's face, for example.
The visual cortex has a map of the visual field on the retina, and in macular degeneration the neurons mapping to the fovea no longer receive input. But several labs, including Kanwisher's, previously found that the neurons in the visual cortex that once responded only to input from central vision begin responding to stimuli at the PRL. In other words, the visual map has reorganized.
"We wanted to know if the chronic, prior use of the PRL causes the cortical change that we had observed in the past, according to what we call the use-dependent hypothesis," said first author Daniel D. Dilks, a postdoctoral fellow in the Kanwisher lab. "Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behavior, according to the use-independent hypothesis?"
The previous studies could not answer this question because they had only tested patients' PRL. This new study tests both the PRL and another peripheral location, using functional magnetic resonance imaging (fMRI) to scan two macular degeneration patients who had no central vision, and consequently had a deprived central visual cortex.
Because patients habitually use the PRL like a new fovea, it could be that the deprived cortex might respond preferentially to this location.
But that is not what the researchers found. Instead, the deprived region responded equally to stimuli at both the preferred and nonpreferred locations.
This finding suggests that the long-term change in visual behavior is not driving the brain's remapping. Instead, the brain changes appear to be a relatively passive response to visual deprivation.
"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex." Kanwisher said. If scientists could one day develop technologies to replace the lost light-sensitive cells in the fovea, patients might be able to recover central vision since the neurons there are still alive and well.
Chris Baker of the Laboratory of Brain and Cognition (NIMH) and Eli Peli of the Schepens Eye Research Institute also contributed to this study, which was supported by the NIH, Kirschstein-NRSA, and Dr. and Mrs. Joseph Byrne.
Adapted from materials provided by Massachusetts Institute of Technology.

MIT study sheds light on brain changes in macular degeneration

2009-03-07T11:05:00.001-08:00

MIT study sheds light on brain changes in macular degeneration
Wednesday, March 4, 2009
CBC News
The brain adapts to find new visual information when a person gets eye disease causing blindness, according to a study from the Massachusetts Institute of Technology.

Researchers found that when people lose their sight because of macular degeneration, the affected neurons simply start seeking visual input from other, non-affected parts of the eye.

Their findings were published Wednesday in the Journal of Neuroscience.

"This study shows us one way that the brain changes when its inputs change. Neurons seem to 'want' to receive input: when their usual input disappears, they start responding to the next best thing," wrote lead researcher Nancy Kanwisher of the McGovern Institute for Brain Research at MIT.

It appears the long-term change in visual behaviour is not driving the brain's remapping; rather, it's the brain's relatively passive response to visual deprivation.

Macular degeneration is the most common form of adult blindness. It affects 800,000 people in Canada. Those suffering from it progressively lose vision in the central visual field of their retina, or their fovea. That means the corresponding part of the visual cortex in the brain also loses input.

"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said in a news release. "If scientists could one day develop technologies to replace the lost light-sensitive cells in the fovea, patients might be able to recover central vision since the neurons there are still alive and well."

Previously, researchers found deprived neurons would begin responding to visual input from another spot on the retina, essentially building a new visual map on the cortex. That information provided evidence of plasticity in the adult cortex. However, there were still questions as to how that happened.

MIT's study sheds light on the underlying neural mechanism.

"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information processing strategy," said Kanwisher.

Typically, people suffering from MD will compensate by using an adjacent patch of undamaged retina. They'll roll their eyes upward to look at someone's face instead of focusing straight on, for instance. That undamaged patch becomes their new "preferred retinal locus," or PRL.

The researchers wanted to find out if the cortical change was caused by chronic prior use of the PRL, said another study author, Daniel D. Dilks, a postdoctoral fellow in the Kanwisher lab.

"Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behaviour," he wrote.

The previous studies could not answer this question because they had only tested patients' PRL. This new study tests both the PRL and another peripheral location, using functional magnetic resonance imaging to scan two macular degeneration patients who had no central vision, and consequently had a deprived central visual cortex.

Because patients habitually use the PRL like a new fovea, it could be that the deprived cortex might respond preferentially to this location.

But that is not what the researchers found. Instead, the deprived region responded equally to stimuli at both the preferred and nonpreferred locations.

Wet and Dry Age-Related Macular Degeneration (AMD)

2009-02-25T11:54:00.001-08:00

The present Competitive Intelligence Report about Wet and Dry Age-Related Macular Degeneration (AMD) provides a competitor evaluation in the field of R&D projects for treatment of AMD as of February 2009.

Macular degeneration in the elderly (“age-related macular degeneration”, AMD) is a major cause of blindness. Its prevalence increases to 30% in patients 75 to 85 years of age. AMD occurs in two forms: dry and wet AMD. Central geographic atrophy, the “dry” form of advanced AMD, results from atrophy to the retinal pigment epithelial layer below the retina, which causes vision loss through loss of photoreceptors (rods and cones) in the central part of the eye. While no treatment is available for this condition, vitamin supplements appear to slow the progression of dry macular degeneration and, in some patients, improve visual acuity. Neovascular or exudative AMD, the “wet” form of advanced AMD, causes vision loss due to abnormal blood vessel growth in the choriocapillaries, ultimately leading to blood and protein leakage below the macula. Bleeding, leaking, and scarring from these blood vessels eventually cause irreversible damage to the photoreceptors and rapid vision loss if left untreated.

It is only recently that new drugs have been approved for wet AMD which halt progression of the visual loss or even lead to improvement. The humanized antibody fragment ranibizumab (Lucentis) directed against vascular endothelial growth factor (VEGF) was developed by Genentech and Novartis has been approved in more than 70 countries worldwide since 2006 and posted record sales of US$ 1.76 bln in 2008.

The proven effectiveness and commercial success of the anti-VEGF treatment of wet AMD has encouraged many companies to develop new treatments of wet AMD based on the proven target VEGF as well as on other experimental approaches (anti-angiogenic, anti-proliferative, anti-inflammatory). More than 20 different approaches are in clinical development and more than 20 preclinical stage projecs are under evaluation for wet AMD. Among the projects are many biologics (antibodies, peptides, proteins, antisense, DNA, cells) facilitated by the topical (intravitreal administration). Small molecule approaches may confer the convenience of oral administration but efficacy still has to be demonstrated. Fewer projects are in clinical development for dry AMD, but the most prominent ones have reached advanced clinical testing, but definitive results are still lacking.

Time course of morphologic effects on different retinal compartments after ranibizumab therapy in age-related macular degeneration.

2009-02-17T17:12:00.000-08:00

Ophthalmology. 2008 Aug;115(8):e39-46.

Ahlers C, Golbaz I, Stock G, Fous A, Kolar S, Pruente C, Schmidt-Erfurth U.

Medical University of Vienna, Vienna, Austria.

PURPOSE: To analyze the effect of ranibizumab therapy on retinal and subretinal compartments in age-related macular degeneration and to compare the time course of compartment specific effects to visual function.

DESIGN: Prospective noncomparative case series.

PARTICIPANTS: Fourteen patients with changes in 3 major compartments owing to neovascular age-related macular degeneration.

METHODS: Standard treatment with 3 monthly doses of intravitreal ranibizumab was performed. Eyes were examined at baseline and weeks 1, 4, and 12 using a standardized protocol. Manual segmentation was applied to all 128 B-scans contained in a macular raster scan (MRS).

MAIN OUTCOME MEASURES: Morphology and time course of different retinal and subretinal compartments.

RESULTS: High-definition optical coherence tomography and manual segmentation allowed for precise identification of volumes within individual compartments. All morphologic parameters responded positively to therapy, but demonstrated a specific time course. Subretinal fluid was identified as the most relevant factor for visual function, whereas changes in retinal and subpigment epithelial volumes did not correlate with the time course of functional rehabilitation.

CONCLUSION: Analysis of MRS identified a characteristic impact of therapy on retinal and subretinal morphology.

PMID: 18675694 [PubMed - indexed for MEDLINE]

Serum Cystatin C Level, Kidney Disease Markers, and Incidence of Age-Related Macular Degeneration

2009-02-12T09:00:00.000-08:00

The Beaver Dam Eye Study

Ronald Klein, MD, MPH; Michael D. Knudtson, MS; Kristine E. Lee, MS; Barbara E. K. Klein, MD, MPH

Arch Ophthalmol. 2009;127(2):193-199.

Objective
To examine the associations of the serum cystatin C level and chronic kidney disease with the incidence of age-related macular degeneration (AMD) over 15 years.

Methods
In this population-based cohort study of 4926 individuals aged 43 to 86 years at baseline, 3779 participated in 1 or more follow-up examinations. Age-related macular degeneration was determined by grading photographs of the macula. Individuals were defined as having mild or moderate to severe chronic kidney disease based on a value of more than 45 mL/min/1.73 m2 to 60 mL/min/1.73 m2 or less and 45 mL/min/1.73 m2 or less, respectively, according to the Modification of Diet in Renal Disease Study equation.

Results
While controlling for age and other risk factors, the level of serum cystatin C at baseline was associated with the incidence of early AMD (odds ratio per log standard deviation [95% confidence interval], 1.16 [1.01-1.35]) and exudative AMD (1.42 [1.03-1.96]) but not geographic atrophy (0.89 [0.56-1.41]) or progression of AMD (1.02 [0.88-1.18]). Mild chronic kidney disease was associated with the 15-year cumulative incidence of early AMD (odds ratio per log standard deviation, 1.36 [95% confidence interval, 1.00-1.86]) but not the incidence of other AMD end points.

Conclusion
There is a relationship between the level of serum cystatin C and chronic kidney disease with the incidence of AMD. The underlying biological processes remain to be determined.

Author Affiliations: Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison.

Age-Related Eye Disease Study (AREDS) Examines Macular Degeneration Risk Related to Cataract Surgery

2009-02-05T15:00:00.000-08:00

Age-related macular degeneration (AMD) and cataract are leading causes of visual impairment in the United States. Both are related to aging, and they share other risk factors, but it has been unclear whether a direct causal link might be involved. Several large epidemiological studies had raised concern that cataract surgery might accelerate AMD progress and threaten vision. To address this concern, Emily Y. Chew, MD, of the National Eye Institute, and colleagues analyzed data for a cohort of participants in the Age-Related Eye Disease Study (AREDS). This cohort is the only large prospective study in which the severity of AMD was documented before and after cataract surgery and which included more than five years of in-depth participant follow-up.

AMD causes changes in the retina, the light-sensitive tissue that focuses images at the back of the eye, and severe AMD leads to loss of central vision. Cataract is cloudiness or opacity in the eye's lens that interferes with the clear focus of images on the retina.

AREDS researchers concluded there was little evidence that cataract surgery had a negative effect on progression to advanced AMD. ?These data may provide some reassurance to patients with AMD who are considering cataract surgery,? Dr. Chew said.

The primary purpose of the AREDS multicenter controlled randomized clinical trial was to assess whether antioxidant and mineral supplements affect progress to advanced AMD and development of cataracts. The cohort study included 4,577 participants (8,050 eyes) aged 55 through 81 at enrollment; it compared the risk of advanced AMD in patients who had cataracts removed versus the risk for those who did not have the surgery. All participants took either antioxidant/mineral supplements or placebos. Study eyes were examined every six months over five or more years. One analysis compared AMD progression in matched pairs of eyes, where one eye had cataract surgery after baseline but before developing advanced AMD, and the paired eye did not have cataract surgery. Matched pairs were determined based on similar risk factors for AMD, assigned antioxidant or placebo treatment, baseline AMD category, person?s age, and other factors. Results of the matched pair analysis and of two other standard analytical models revealed no consistent pattern of accelerated AMD progression after cataract surgery.

Several factors may explain the divergent conclusions reached by AREDS and the earlier studies. The most likely cause would be that earlier studies had unintended biases or confounding variables. Also, techniques of cataract surgery and lens replacement have changed over time, and AREDS participant surgeries were performed more recently than those tracked in the combined-population studies. A significant number of subjects in earlier studies did not have lens replacement after cataract extraction, while AREDS participants were likely to have had ultraviolet-B light blocking lenses inserted, which may have protected their maculae and decreased AMD risk.

Neurotech's ECT Technology Wants to Rid the World of Intraocular Problems

2009-01-28T10:20:00.000-08:00

Neurotech Pharmaceuticals, Inc., a Lincoln, Rhode Island based firm, has announced that the FDA has granted Fast Track designations for the firm's lead product candidate, the NT-501, for treatment of visual loss in two indications: retinitis pigmentosa (RP) and dry form of age-related macular degeneration (dry AMD). Such designations should allow the company to accelerate clinical development of its continuous, long-term release formulation of the therapeutic protein Ciliary Neurotrophic Factor (CNTF), designed to be released into the vitreous body from a proprietary Encapsulated Cell Technology (ECT) device.

More about Neurotech's technology platform and the NT-501:

Neurotech's core technology platform is Encapsulated Cell Technology (ECT), a unique technology that allows for the long term, sustained delivery of therapeutic factors to the back of the eye.

ECT implants consist of cells that have been genetically modified to produce a desired therapeutic factor that are encapsulated in a section of semi-permeable hollow fiber membrane. The diffusive characteristics of the hollow fiber membrane are designed to promote long-term cell survival by allowing influx of oxygen and nutrients while simultaneously preventing direct contact of the encapsulated cells with the cellular and molecular elements of the immune system. The cells continuously produce the therapeutic protein which diffuses out of the implant at the target site. ECT therefore enables the controlled, continuous delivery of therapeutic factors directly to the retina, bypassing the blood-retina barrier. Long-term protein delivery (18 months) in the vitreous cavity of the eye has consistently been achieved when ECT devices containing human cells genetically engineered to secrete CNTF have been implanted in a highly disparate mammalian species (rabbits). In addition, the implants can be retrieved, providing an added level of safety as well as the ability to reverse or adjust therapy, if needed.

ECT based products can be tailored to address the three main clinical manifestations of retinal diseases: degeneration of photoreceptors and/or ganglion cells in the neural retina, vascular proliferation and inflammation. A number of proteins have been discovered in the field of ophthalmology that possess powerful neurotrophic, anti-angiogenic and anti-inflammatory properties. These proteins have the potential to significantly slow or halt disease processes in the eye. ECT represents a unique platform for the safe and effective delivery of various factors for the treatment of these chronic ophthalmic diseases as follows:

# neurotrophic factors for the treatment of retinal degeneration in Retinitis Pigmentosa (RP), Geographic Atrophy (serious condition associated with the Dry form of Age-related Macular Degeneration), Glaucoma, Retinal Vein Occlusion and others.

# anti-angiogenic factors for the treatment of vascular proliferation in Diabetic Retinopathy and the Wet form of AMD, and for the treatment of abnormal vascular permeability for various forms of Macular Edema.

# anti-inflammatory factors for the treatment of Ocular Inflammations (Uveitis)

The current product is 6 mm in length and consists of genetically-modified human cells packaged in a semi-permeable hollow fiber membrane with a suture loop at one end to anchor the implant to the sclera. In contrast to gene therapy, ECT does not modify the host genome. The implant is surgically placed in the vitreous body. The implant is sutured in a manner that allows for its retrieval when desired. The surgical procedure is performed as an out-patient procedure in about 20 minutes...

... NT-501, consists of encapsulated human cells genetically modified to secrete ciliary neurotrophic factor (CNTF). NT-501 is designed to continually deliver a low, safe and therapeutic dose of CNTF, a well-established neurotrophic factor, into the back of the eye. The Company believes that CNTF activates dying retinal photoreceptors and protects them from degeneration.

FDA OKs First Human Trials of Embryonic Stem Cells

2009-01-24T15:53:00.001-08:00

By Alexis Madrigal
January 23, 2009 | 4:10:36 PM

The Federal Drug Administration has approved the first human trials of embryonic stem cells — a sign of a new, liberal attitude toward stem cell research, which was hamstrung by the Bush administration.

Starting this summer, the biotech firm Geron will treat a small group of spinal-cord injury patients using neurons derived from stem cells, marking the first time embryonic stem cells will be tested in humans.

The trial is designed to test the safety of the treatment, not how well it works. Nonetheless, it's a huge first step for the field.

"It signals to me that we have the primary regulatory authorities on board for embryonic stem cells," said Alan Trounson, president of the California Institute of Regenerative Medicine, a $3 billion state initiative to support stem cell research. "That really is a tremendous piece of news."

Under the Bush administration, stem cell research was slowed by an executive order, signed in August 2001, that (severely) restricted the types of stem cells and stem cell research that could be conducted. President Barack Obama is widely expected to lift Bush’s executive order, perhaps as soon as next week.

Working in a handful of medical centers around the country, Geron will treat eight to 10 recent paraplegics, who can use their arms but not their legs. The patients will receive an injection of neurons to the site of the damage, followed by a short treatment of anti-rejection drugs.

Previous animal studies suggest the new neurons will repair damaged neurons and secrete substances to help nerves function and grow.

Amy Rick, president of Coalition for the Advancement of Medical Research, a group of dozens of research institutions that support stem cell research, said the Geron trial is a milestone.

"It's hugely significant in the sense that it's the first approval of a human embryonic stem cell trial," she said. "In this week of hope and change, it feels even better."

While Geron scientists waited months for FDA approval of the stem cell treatment, they are reluctant to link the go-ahead directly to the inauguration of Obama.

A Geron spokeswoman said that the company had no evidence of political influence aiding their application.

“It’s just coincidental timing,” the spokeswoman said.

Karen Riley, an FDA spokeswoman, echoed that the timing was coincidental. "We make science-based decisions and politics is not a factor," she said.

But the new president surely didn't hurt matters. The chairman of Trounson's organization told the New York Times, "I think this approval is directly tied to the change in administration."

The approval is expected to the first of several trials involving embryonic stem cells. A recent CAMR report found that nine companies, including Geron, were in the process of developing human embryonic stem cell treatments.

Embryonic stem cells are like blank slates that can be transformed into different types of tissue. They've been hailed as the next big thing in medicine ever since University of Wisconsin scientist James Thomson showed their ability to regenerate in 1998. Since then, stem cells have been like a high school star turned NBA draft pick — talented and expensive but undisciplined and perhaps not quite ready for the glare of the big game. Like many biotechnology techniques, the lag between scientific discovery and clinical treatment can be decades.

Still, the Regenerative Medicine Institute’s Trounson, who was a stem cell scientist in Australia before heading the California institute, said that experimental treatments are outpacing his expectations.

"We're running an agency funding this work and I'm astounded at what's happening in this space,” he said.

Trounson said there’s evidence in animal trials that stem cells are effective in treating ailments as varied as diabetes, Alzheimers, multiple scleorsis and macular degeneration.

“It’s just fantastic,” Trounson said. "And I would expect some of these to enter clinical trials sooner, rather than later."

His agency expects to fund up to a dozen scientists who think they can submit their stem cell work to the FDA for clinical trial approval within four years.

From there, those so-called investigational new drugs will have to follow the path that Geron's treatment did. The company submitted its application early in 2008. It was then put on hold in May 2008 and kicked back to the company for further review. Seven months later, the company resubmitted the application and received approval Wednesday, the day after the inauguration.

That said, Obama's political influence is likely to invigorate a field that — despite impressive state-level and private efforts — has been ham-strung by Federal regulation and the specter of increased government regulation.

"With President Obama there, there will be a big change not only in government administration and the public sector, but I think it will encourage the pharmaceutical companies to be involved as well," Trounson said.

International Stem Cell Begins Pre-Clinical Testing of Its Parthenogenetic Stem Cells for Treatment of Retinal Disease First Company To Grow Human Cor

2009-01-14T11:09:00.000-08:00

OCEANSIDE, Calif., Jan 13, 2009 (BUSINESS WIRE) -- International Stem Cell Corporation has created layered human tissue from its unique parthenogenetic stem cells and transplanted this tissue into animals in pre-clinical trials to establish a potential new treatment for human retinal diseases, such as macular degeneration or retinitis pigmentosa.

"Intact layers of retinal progenitor cells have been shown to restore lost visual responses in several retinal degeneration rodent models," said Dr. Hans Keirstead, Co-Director of the Sue and Bill Gross Stem Cell Research Center at the University of California, Irvine. "Thus, we are developing intact retinal layers derived from International Stem Cell's human parthenogenetic stem cells which could become a sustainable, FDA-approved therapeutic supply for patients with retinal degenerative diseases."

ISCO's human parthenogenetic stem cells have the potential to treat human disease yet possess key medical and ethical advantages over other kinds of stem cell products. They can be matched to common immune types and thus reduce the chance of transplant rejection among large segments of the population. Because they are created from unfertilized human eggs, they do not require the destruction of human embryos.

"We are aggressively pushing forward safe treatments for human diseases using parthenogenetic stem cells," said Jeffrey Janus, President of International Stem Cell. "If we are successful in this work, our next step is to manufacture this layered human tissue for further tests, including human trials. This illustrates the strengths of combining scientific collaborations with outside researchers such as Dr. Keirstead with ISCO's science and cell manufacturing expertise."

For more information, visit the ISCO website at: www.internationalstemcell.com.

Protein Might One Day Prevent Blindness

2009-01-09T12:42:00.000-08:00

01.07.09, 08:00 PM EST
Researchers find it prolongs lives of key vision cells in mice

THURSDAY, Jan. 8 (HealthDay News) -- Researchers working with mice have identified a protein that appears to prolong the lives of retinal cells in both healthy and diseased eyes.

The discovery could one day lead to treatments that would prevent blindness among people genetically predisposed to develop retinal disease, the scientists said.

The protein, known as histone deacetylase 4 (HDAC4), is naturally produced by both mice and humans and is typically involved in the regulation of bone and muscle development.

Reducing the amount of HDAC4 to below-normal levels appears to lead to premature photoreceptor cell death in healthy eyes, the study revealed. In contrast, increasing quantities of this protein to above-normal levels appears to protect the lifespan of these critical vision cells -- both in healthy mouse eyes and in those mice suffering from a genetic flaw, also present in humans, that gives rise to degenerative retinal disease.

The finding -- if replicated in people -- could ultimately lead to new interventions to prevent such disease-driven blindness, or even to the development of methods to restore lost sight to diseased retinas.

"There are some inherited genetic defects that lead to the death of the two types of photoreceptor cells in the eye that capture light, first directly killing the rod cells and then the cone cells which depend on rod cell survival," explained study author Bo Chen, a postdoctoral research fellow with the Howard Hughes Medical Institute at Harvard Medical School in Boston. "So, this mutation eventually leads to complete blindness."

"But what we found," Chen noted, "is that we could actually promote the survival of these genetically affected photoreceptors by introducing more of this particular protein, even though the photoreceptors themselves continue to remain genetically defective."

Chen and his colleagues report their findings in the Jan. 9 issue of Science.

The findings are based solely on a series of neural cell experiments, focused on the retinal health of live mice, that were designed to assess the impact of both under-expression and overexpression of the HDAC4 protein.

Subsequent lab work led the researchers to determine that in sufficient quantities the protein indeed displays a protective effect against eye cell death and thereby has an "essential role in neuronal survival," they wrote.

Yet despite expressing enthusiasm for his current work, Chen emphasized the ongoing nature of the effort.

"Even though the genetics are the same in mice and humans, at this stage it's really very experimental," he stressed. "And much more work needs to be done before we know this will be efficacious in humans."

Nevertheless, Dr. Robert Cykiert, a clinical associate professor of ophthalmology at New York University Langone Medical Center in New York City, described the current work as an "impressive" effort.

"Clearly a lot of people go blind from retinal diseases," he said, noting that glaucoma and macular degeneration are two serious conditions that result from retinal cell death. "And this protein they worked with appears to be what we call neuro-protective, in that it has protective benefits on both the photoreceptor layer that gets damaged in macular degeneration as well as on the ganglion cell layer which is damaged by glaucoma. So this finding could actually turn out to be a major accomplishment, affecting a lot of patients down the road."

However, Rando Allikmets, an associate professor of ophthalmology, pathology and cell biology at Columbia University in New York City, took Chen's cue in cautioning that the true measure of the current work awaits human clinical trials.

"It's a very good study, an interesting observation and a very encouraging finding that will definitely lead to an investigation of this pathway for possible therapeutic targets," he said. "But the problem is that they have identified a protein involved with very basic functions -- including muscle development and bone growth -- so it's very difficult to predict if what they did in mice can be done in humans at all and, even if it can, if it will work in the same way."

Cykiert agreed.

"Of course, it's a mouse study," he acknowledged. "So you certainly don't know if what they've found will be reproduced in patients. And in any case, it would take 10 years to develop any drugs from this that might benefit people. So, yes, it's just a first step."

In vivo 3D cellular imaging of eyes is aim of extended research grant

2009-01-03T10:55:00.000-08:00

DECEMBER 30, 2008--The National Eye Institute (Bethesda, MD) has awarded a $5 million research grant to ophthalmologist John S. Werner of the University of California-Davis and researchers at three other universities. The grant will fund continued development of technology for three-dimensional imaging of cells in the living eye.

The studies, part of the next five-year phase of a Bioengineering Research Partnership, could benefit increasing numbers of patients suffering from glaucoma and age-related macular degeneration. Cell-level imaging of eyes would provide significant advances in understanding the origins of retinal and optic nerve disease and in evaluating novel therapies for a wide spectrum of blinding diseases.

"Our project has been described as the Hubble telescope of the eye," said Werner, the project's principal investigator and a professor at the UC Davis Health System Eye Center.

"Vision and visual disorders begin at the cellular and molecular levels, yet the ability to visualize most cellular structures in vivo continues to elude scientists and clinicians," said Werner, whose research interests include changes in vision across the life span and diseases of the retina and optic nerve. "Despite extraordinary advances in retinal imaging, only a small fraction of human retinal cells have been visualized in the living eye."

The first phase of the partnership, started in 2003, combined adaptive optics and optical coherence tomography (OCT) to provide high-lateral and high-axial resolution, respectively. The initial phase also was funded by a five-year, $5 million grant from the National Eye Institute.

Led by Werner, investigators used this new instrumentation to create volume images of structures previously only visible with histology, including the photoreceptor outer segments, Fibers of Henle, individual optic nerve fiber bundles, detailed structures within the drusen, or lesions, of macular degeneration patients, and the fine structure of the lamina cribosa of the optic nerve. They developed instrumentation with sufficient resolution to image all the major retinal neurons in three dimensions.

However, while the resolution of their instruments reached the cellular scale, many cells and structures of interest were of low contrast. As a result, the major engineering focus of the next five years will be on contrast enhancement through additional imaging techniques. The resulting adaptive optics and optical coherence tomography instruments will permit human in vivo imaging with sufficient resolution and contrast to visualize the smallest of cells in the human retina.

Partner institutions include Duke University, Department of Bioengineering; Indiana University, Department of Optometry; and Lawrence Livermore National Laboratory, Physics and Advanced Technologies Section.

The project's engineering aims have parallel clinical/vision science objectives, including advancing the understanding of changes in cell layers associated with the most common worldwide diseases leading to blindness, including age-related macular degeneration and glaucoma.

More information:
John Werner's Vision Science and Advanced Retinal Imaging lab

PSivida's eye treatment in trials for macular degeneration

2008-12-27T20:49:00.000-08:00

By Mass High Tech staff

PSivida Ltd., an Australian drug company with U.S. headquarters in Watertown, has announced that its Medidur technology, licensed to Alimera Sciences Inc., has begun an early-stage clinical trial for treating macular degeneration. The technology is currently in Phase 3 clinical trials for treating a different disease associated with blindness, diabetic macular edema.

Medidur is a tiny insert, injected during an in-office procedure, which is being studied as a way to deliver a low dose of fluocinolone acetonide, a corticosteroid, to the retina for up to three years as a treatment for DME. To be marketed by Alimera, a privately held ophthalmic pharmaceutical company, the product will go by the name Iluvien if it is approved by the U.S. Food and Drug Administration, pSivida (Nasdaq: PSDV) (ASX: PSD) (FSE: PSI) officials said.

The study is expected to evaluate the effectiveness of Illuvien in treating dry-age related macular degeneration in patients with bilateral geographic atrophy.

In a previous study conducted on animals, Iluvien showed signs of preventing macular degeneration.

Alimera Sciences and pSivida have a worldwide agreement to co-develop and market the Medidur insert for the use of fluocinolone acetonide to treat DME. The agreement also includes the option to identify other compounds for ophthalmic diseases, potentially resulting in three additional products with the Medidur insert.

PSivida's eye treatment in trials for macular degeneration

2008-12-16T08:54:00.000-08:00

By Mass High Tech staff

PSivida Ltd., an Australian drug company with U.S. headquarters in Watertown, has announced that its Medidur technology, licensed to Alimera Sciences Inc., has begun an early-stage clinical trial for treating macular degeneration. The technology is currently in Phase 3 clinical trials for treating a different disease associated with blindness, diabetic macular edema.

Medidur is a tiny insert, injected during an in-office procedure, which is being studied as a way to deliver a low dose of fluocinolone acetonide, a corticosteroid, to the retina for up to three years as a treatment for DME. To be marketed by Alimera, a privately held ophthalmic pharmaceutical company, the product will go by the name Iluvien if it is approved by the U.S. Food and Drug Administration, pSivida (Nasdaq: PSDV) (ASX: PSD) (FSE: PSI) officials said.

The study is expected to evaluate the effectiveness of Illuvien in treating dry-age related macular degeneration in patients with bilateral geographic atrophy.

In a previous study conducted on animals, Iluvien showed signs of preventing macular degeneration.

Alimera Sciences and pSivida have a worldwide agreement to co-develop and market the Medidur insert for the use of fluocinolone acetonide to treat DME. The agreement also includes the option to identify other compounds for ophthalmic diseases, potentially resulting in three additional products with the Medidur insert.

Clinical Trial for Macular Degeneration Seeks a New Way of Seeing

2008-12-12T19:30:00.000-08:00

Published on 10 December 2008, 09:40 Last Update: 2 day(s) ago by Insciences

The brain's remarkable ability to reorganize itself to compensate for vision loss, the ability called plasticity, may be the key in helping those with age-related macular degeneration (AMD) see better. This theory is the impetus behind a study between Emory Eye Center and the Georgia Institute of Technology (Psychology). Patients who have retinal damage because of AMD sometimes begin to see by using other parts of the intact retina. By "training" these patients to focus on using those good retinal cells, they may experience increased visual acuity.

Susan Primo, OD, MPH, of Emory Eye Center, says the Phase 2 portion of the clinical trial "Age-Related Macular Degeneration and Cortical Reorganization" will help bridge the knowledge gap between cortical plasticity and visual function.

"Results from these studies will begin to provide answers for how behavioral improvements in AMD patients can lead to changes in underlying brain activity and, most importantly, how we can influence those changes to maximize use of remaining vision," Primo says. "Once this link is made, clinicians and healthcare engineers can use the information to design and implement rehabilitation therapies and technologies that will expedite efficient use of fixation strategies ultimately fostering cortical reorganization."

Age-related macular degeneration is the leading cause of blindness in the elderly, accounting for 10 million people who have reduced vision in the United States (Research to Prevent Blindness). AMD is a disease associated with aging that gradually destroys sharp, central vision. Central vision is needed for seeing objects clearly and for common daily tasks such as reading and driving. People in middle-age have about a 2 percent risk of getting AMD, but this risk increases to nearly 30 percent in those over age 75. More than 200,000 develop AMD each year in this country.

"Visual rehabilitation is entering an exciting area of research that expands our current understanding of neuroplasticity of the visual system," says Timothy W. Olsen, director of Emory Eye Center and a retina specialist. "Findings from this study and others may help us understand the tremendous capacity of our central nervous system, especially as it relates to sensory deficits. Combining expertise of the Emory Eye Center with Georgia Tech opens exciting new opportunities in vision research."

Phase 1 of the study appears in the December edition of the journal Restorative Neurology and Neuroscience (Restor Neurol Neurosci. 2008;26(4-5):391-402.)

Phase 1 of the trial at Emory involved seven patients, and the Phase 2 portion at Emory will have 10 patients. The goal will be to study hundreds of patients in the near future. Results will be disseminated in late 2009.

Funding is provided through the Health Systems Institute Seed Grant, a collaboration between Georgia Institute of Technology and Emory University/Children's Healthcare of Atlanta/Egleston. The HSI Seed Grant supports collaborative and interdisciplinary research projects that will help stimulate innovative healthcare research and promote improvements in healthcare. The seed grant awards are specifically designed to provide funding for novel projects that demonstrate a high potential for enhanced diagnostic capabilities of diseases, lead to new inventions that yield new patents, licenses and/or commercial products, lead to high quality peer-reviewed publications and those with high potential to leverage seed funding into extra-mural support.

About Emory Eye Center: The Department of Ophthalmology and Emory Eye Center have a mission to conduct pioneering research into blinding eye diseases, to educate and train eye professionals, and to provide excellent patient care. The Department includes 35 ophthalmologists, seven optometrists, nine basic scientists, 11 post-doctoral fellows, and nine researchers in other Emory departments who hold joint appointments in the Department of Ophthalmology. Ophthalmology research is supported by $6 million in NIH funding. The Department remains in the top rankings (#9 -- 2008) by U.S. News & World Report for the 12 years the magazine has held a ranking for Ophthalmology. It also ranks in the Top Ten in all four categories surveyed by Ophthalmology Times annual report.

The Robert W. Woodruff Health Sciences Center of Emory University is an academic health science and service center focused on missions of teaching, research, and health care. Its components include schools of medicine, nursing, and public health; the Yerkes National Primate Research Center; the Emory Winship Cancer Institute; and Emory Healthcare, the largest, most comprehensive health system in Georgia. The Health Sciences Center has a $2.3 billion budget, 17,000 employees, 2,300 full-time and 1,900 affiliated faculty, 4,300 students and trainees, and a $4.9 billion economic impact on metro Atlanta.

Contacts: Joy Bell, Tel: 404-778-3711

Source: Emory University

Study Shows Lutein and Zeaxanthin Protect Against Age-Related Macular Degeneration

2008-12-09T08:51:00.000-08:00

by David Gutierrez, staff writer

(NaturalNews) Researchers from Ohio State University may have discovered a mechanism by which proteins known as xanthophylls help prevent against age-related vision loss, they reported in a study published in the Journal of Lipid Research.

"Our research to understand this mechanism might provide a greater appreciation for how one could intervene to possibly slow macular degeneration," said senior study author Earl Harrison.

Age-related macular degeneration is one of the most common causes of age-related vision loss and affects approximately 10 million people in the United States. The deterioration of the macula, a tissue located in the center of the retina, causes vision in the center of the eye to blur, which lead to functional blindness. The condition cannot be reversed once it develops; it can only be slowed.

Prior research has suggested that the xanthophyll proteins lutein and zeaxanthin may protect against the eight-related macular degeneration by filtering out potentially harmful light from the blue end of the spectrum and also protecting the eye against damage from oxidation. The two proteins have been observed to concentrate in the macula, forming a yellow spot.

In the current study, researchers tested the hypothesis that the xanthophylls are transported to the macula by proteins known as scavenger receptor class B, type 1 (SR-B1). They treated pigment cells from the lining of the human retina with lutein, zeaxanthin and the related compounds beta-carotene, finding that the cells absorbed more xanthophylls than they did beta-carotene.

The researchers then blocked the action of SR-B1 by one of two methods. Both of the methods led to a decrease in xanthophyll of distortion of 41 to 87 percent.

Lutein and zeaxanthin cannot be synthesized by the body, but must be consumed in foods such as green, leafy vegetables, peas, summer squash, or yellow and orange fruits and vegetables (including carrots, papaya and peaches).

Sources for this story include: www.sciencedaily.com.

Avastin problems crop up for eye patients

2008-12-07T09:26:00.001-08:00

'They’re taking it out of its (original) packaging, repackaging it and injecting it into people’s eyes'

By HELEN BRANSWELL The Canadian Press

TORONTO — Public health authorities in Canada are investigating a spike in cases of eye inflammation among patients being treated for macular degeneration with the cancer drug Avastin.

First noticed in British Columbia, there appears to be a rise in cases in other parts of the country as well.

And now authorities are trying to draw the potential problem to the attention of the global public health community in the hopes of seeing if it is being observed elsewhere.

The problem is believed to stem from a particular lot of the drug that was distributed widely around the world, though not to the United States. The lot number is B3002B028.

The drug’s manufacturer, the Swiss pharmaceutical firm Roche, is co-operating with Health Canada and the British Columbia Centre for Disease Control, which was alerted to the problem by ophthalmologists.

The situation puts Roche in an awkward position. Avastin is a colon cancer drug; it is not approved for use as a treatment age-related macular degeneration.

And Roche doesn’t want to encourage the off-label use of the drug by ophthalmologists who have embraced it as a much cheaper alternative to a similar drug, Lucentis, which has been approved as a treatment for macular degeneration.

"Absolutely we do not recommend this," said Samantha Ouimet, a spokeswoman for Roche Canada.

"They’re taking it out of its (original) packaging, repackaging it and injecting it into people’s eyes. This comes in a bag and it’s meant for intravenous use for people with cancer."

Ouimet said the company is in discussions with Health Canada. But it is reluctant to put out an advisory warning people not to use the drug as a treatment for age-related macular degeneration when the drug was never approved for this purpose.

Any statement could be seen as promoting the off-label use, Ouimet said.

"Is it a delicate situation? Absolutely."

Ophthamologists in British Columbia started noticing a problem in October.

A small portion — under two per cent — of people treated for age-related macular degeneration with Avastin will develop acute intra-ocular inflammation. But between Oct. 3 and Oct. 27, the rates were much higher.

The BC CDC was called in to help investigate the cluster of cases. And they concluded that the rate of inflammation among patients treated with Avastin from the lot in question was almost 10 times higher than the normal rate. The lot is no longer in use there.

Dr. David Patrick, the centre’s director of epidemiology services, submitted a report on the investigation to ProMED, an electronic reporting system that sends out alerts about outbreaks to a mailing list of public health officials, scientists and other interested parties around the world.

Patrick said the team investigating the issue sent out feelers to ophthamologists in about a half-dozen other Canadian centres and has heard back that others too have noticed an increase in cases of inflammation after use.

The inflammation causes cloudy vision, but appears to clear up over time, he said.

Ouimet said there have been no reports of problems from other countries — and no reports of adverse reactions in cancer patients who received treatments from the same lot.

"We have reviewed all the analytical release data for the lot in question. And all the best parameters were within the limits for use in oncology," she said.

"So we found no deviations in the manufacturing process. All the environmental testing was fully compliant. We’ve revisited the batch. It is safe . . . for its indicated purpose."

Patrick said scientists at the University of British Columbia are studying vials of the drug. But so far they haven’t found anything usual.

"On the initial go-through they haven’t determined a chemical difference between the implicated lot and another one. But there may well be further work with that," he said.

Brain Reorganizes To Adjust For Loss Of Vision

2008-11-22T17:25:00.000-08:00

Article Date: 21 Nov 2008

A new study from Georgia Tech shows that when patients with macular degeneration focus on using another part of their retina to compensate for their loss of central vision, their brain seems to compensate by reorganizing its neural connections. Age related macular degeneration is the leading cause of blindness in the elderly. The study appears in the December edition of the journal Restorative Neurology and Neuroscience.

"Our results show that the patient's behavior may be critical to get the brain to reorganize in response to disease," said Eric Schumacher, assistant professor in Georgia Tech's School of Psychology. "It's not enough to lose input to a brain region for that region to reorganize; the change in the patient's behavior also matters."

In this case, that change of behavior comes when patients with macular degeneration, a disease in which damage to the retina causes patients to lose their vision in the center of their visual field, make up for this loss by focusing with other parts of their visual field.

Previous research in this area showed conflicting results. Some studies suggested that the primary visual cortex, the first part of the cortex to receive visual information from the eyes, reorganizes itself, but other studies suggested that this didn't occur. Schumacher and his graduate student, Keith Main, worked with researchers from the Georgia Tech/Emory Wallace H. Coulter Department of Biomedical Engineering and the Emory Eye Center. They tested whether the patients' use of other areas outside their central visual field, known as preferred retinal locations, to compensate for their damaged retinas drives, or is related to, this reorganization in the visual cortex.

The researchers presented 13 volunteers with a series of tests designed to visually stimulate their peripheral regions and measure brain activity with functional magnetic resonance imaging. They found that when patients visually stimulated the preferred retinal locations, they increased brain activity in the same parts of the visual cortex that are normally activated when healthy patients focused on objects in their central visual field. They concluded that the brain had reorganized itself.

The parts of the visual cortex that process information from the central visual field in patients with normal vision were reprogrammed to process information from other parts of the eye, parts that macular degeneration patients use instead of their central visual areas.

While there is evidence with other tasks that suggests that the brain can reorganize itself, this is the first study to directly show that this reorganization in patients with retinal disease is related to patient behavior.

The research group is currently studying how long this reorganization takes and whether it can be fostered through low-vision training.

The research was funded in part by a seed grant from the Georgia Tech/Emory Health Systems Institute

StemCells, Inc. Announces Preclinical Results Showing its Proprietary Human Neural Stem Cells Can Prevent Vision Loss

2008-11-22T17:23:00.000-08:00

StemCells, Inc reported today that its proprietary HuCNS-SC(R) product candidate (purified human neural stem cells), when transplanted into a well-established animal model, can protect the retina from progressive degeneration. Retinal degeneration leads to loss of vision in diseases such as age-related macular degeneration and retinitis pigmentosa. This promising study was conducted by Dr. Raymond Lund, a researcher and professor at the Casey Eye Institute at Oregon Health & Science University (OHSU) and his research team. Dr. Lund will present the study results at a seminar sponsored by the Foundation Fighting Blindness on Saturday, November 1, 2008. The seminar is scheduled to begin at 9:00 a.m. and will be held at the University of California -- San Francisco, Cole Hall (Medical Sciences Building on Parnassus Campus) in San Francisco, California.

"This study confirms the results of previously published academic studies evaluating neural stem cell transplantation into the retina and provides us with the rationale to pursue clinical testing of HuCNS-SC cells for retinal disorders," said Stephen Huhn, MD, FACS, FAAP, Vice President and Head of the CNS Program at StemCells, Inc. "We are already conducting additional preclinical studies and a pre-IND meeting has been scheduled with the FDA for December of this year to determine the pathway to a successful IND filing."

In this preclinical study, Dr. Lund and his co-investigator at OHSU, Dr. Peter Francis, transplanted HuCNS-SC cells into the Royal College of Surgeons (RCS) rat, a well established animal model of retinal degeneration. In the RCS model, a genetic mutation causes dysfunction of the retinal pigmented cells. Dysfunction in these cells, whose normal function is to support photoreceptors in the eye, causes progressive loss of the photoreceptors and degeneration of the retina, and ultimately, loss of visual function. Photoreceptor loss in the RCS rat begins as early as three weeks of age and by 24 weeks all photoreceptors are typically lost. In the study, the researchers transplanted HuCNS-SC cells into one eye of 21-day-old RCS rats while keeping the opposite eye as the control. Animals were evaluated starting at day 40 (19 days post transplant) and then at routine intervals up to 150 days post transplant. The evaluations showed that the HuCNS-SC cells survived the transplants and engrafted, and the eyes transplanted with the cells showed preservation of the photoreceptors and stabilization of visual function.

"The HuCNS-SC cell has proven to have very robust survival, preserving vision in our rat model at time points beyond six months," commented Dr. Lund. "These data are very encouraging and suggest cell-based therapies for retinal degeneration can be a viable treatment approach."

Dr. Francis, a retina specialist and researcher, added, "I am excited by our burgeoning collaboration with StemCells. The results of the early preclinical studies support the potential for these cells to treat retinal degenerative disease. I am especially excited by the fact that the cell is currently being tested in a clinical trial for Batten disease, a disorder of the central nervous system, which should make the transition from the laboratory to clinical use in retinal disease that much easier."

Dr. Lund received his PhD in Anatomy from University College London, after which he joined the faculty and received tenure within two years. Shortly thereafter, he moved to the United States, joining the faculty at Stanford University. Throughout his career, Dr. Lund has held several impressive academic positions including Chair of the Anatomy Department at the Medical University of South Carolina, Chair of the Neurobiology and Anatomy Department at the University of Pittsburgh, chair of the Anatomy Department at the University of Cambridge in England, the Duke Elder Professorship at the Institute of Ophthalmology in London, and the Calvin and JeNeal Hatch Chair of Ophthalmology at the Moran Eye Center at the University of Utah. In 2005, he was appointed Vice Chair of research at the Moran Eye Center in Utah. In 2007, Dr. Lund was recruited to join the faculty of the Oregon Retinal Degeneration Center at the Casey Eye Institute.

Throughout his career, Dr. Lund's research has centered on the response of the central nervous system to injury and mechanisms of rescue and repair. Focusing on the retina and its connections with the brain, he pioneered eye transplants in mammals in the late 1970s. Currently, he is investigating the use of cell-based therapies for photoreceptor degeneration in animal models of human disease.

Dr. Francis is an ophthalmologist and retina specialist at the Casey Eye Institute, and an Associate Professor, Oregon Health & Science University. Dr. Francis received his MD from University of Southampton, Southampton, England, and his PhD in molecular genetics at the Institute of Ophthalmology in London. He co-directs the Casey Macular Degeneration and Oregon Retinal Degeneration Centers. His clinical and research interests have focused on age-related macular degeneration and inherited retinal disorders.

About Retinal Degeneration
The retina is a thin layer of neural cells that lines the back of the eye and is responsible for converting external light into neural signal processed by the brain. The loss of function in retinal cells leads to an impairment or loss of vision. The macula, one of the most critical parts of the retina, is responsible for processing detailed vision. The most common forms of retinal degeneration are age-related macular degeneration and retinitis pigmentosa. In the United States, age-related macular degeneration affects over 1.7 million people in the over-65 population and is the leading cause of blindness in that group. Retinitis pigmentosa is a class of hereditary diseases that also leads to progressive degeneration of retinal cells. In the United States, the most common types of retinitis pigmentosa affect approximately 65,000 people. Preventative measures for both age-related macular degeneration and retinitis pigmentosa have limited impact on the disease and current treatments are not curative.

About HuCNS-SC Cells
StemCells' lead product candidate, HuCNS-SC cells, is a purified composition of normal human neural stem cells that are expanded and stored as banks of cells. The Company's preclinical research has shown that HuCNS-SC cells can be directly transplanted; they engraft, migrate, differentiate into neurons and glial cells; and they survive for as long as one year with no sign of tumor formation or adverse effects. These findings show that HuCNS-SC cells, when transplanted, act like normal stem cells, suggesting the possibility of a continual replenishment of normal human neural cells.

About StemCells, Inc.
StemCells, Inc. is a clinical-stage biotechnology company focused on the discovery, development and commercialization of cell-based therapeutics to treat diseases of the central nervous system and liver. The Company's product development programs seek to repair or repopulate CNS and liver tissue that has been damaged or lost as a result of disease or injury. StemCells has pioneered the discovery and development of HuCNS-SC(R) cells, its highly purified, expandable population of human neural stem cells. StemCells has completed enrollment and dosing of a six patient Phase I clinical trial of its proprietary HuCNS-SC product candidate as a treatment for neuronal ceroid lipofuscinosis (NCL) and expects the trial to be completed in January 2009. NCL, which is often referred to as Batten disease, is a rare and fatal neurodegenerative disease that affects infants and young children. StemCells owns or has exclusive rights to more than 50 issued or allowed U.S. patents and more than 150 granted or allowed non-U.S. patents. Further information about the Company is available on its web site at: www.stemcellsinc.com.

About OHSU and Casey Eye Institute
Oregon Health & Science University is Oregon's only health and research university and the state's only academic health center. OHSU is Portland's largest employer and the fourth largest in Oregon (excluding government), with more than 12,400 employees. OHSU's size contributes to its ability to provide many services and community support activities not found anywhere else in the state. It serves patients from every corner of the state, and is a conduit for learning for more than 3,400 students and trainees. OHSU is the source of more than 200 community outreach programs that bring health and education services to every county in the state.

The Casey Eye Institute, named after the founders of United Parcel Service, opened on the OHSU Marquam Hill Campus in 1991. The Casey Eye Institute is an academic regional eye center dedicated to preventing blindness through research, and to bringing advanced technology to the Pacific Northwest through continuing education of physicians. Casey is the seventh and final regional eye research center in the nation sponsored by Research to Prevent Blindness, the world's leading voluntary organization in support of eye research.

Research in mice raises question about macular degeneration drugs

2008-11-22T17:21:00.000-08:00

Posted by Elizabeth Cooney November 7, 2008 11:05 AM

A drug used to choke new blood vessel growth in the eye disease macular degeneration may damage cells crucial to vision, if research done in mice carries over to humans, Harvard researchers report in the online journal PLoS One.

A team from the Schepens Eye Research Institute and Harvard Medical School studied what happened when levels of vascular endothelial growth factor, or VEGF, were tamped down in they eyes of adult mice. Drugs that block VEGF reduce the excess blood vessel growth and leakage that characterize macular degeneration. The researchers also found that lowering VEGF affected cells not involved in blood vessel growth but in visual function.

“The take-home message of this study is that physicians should be vigilant in monitoring patients undergoing anti-VEGF treatments for any possible signs of these side effects,” senior author Dr. Patricia D’Amore said in a statement. “Drugs such as Lucentis are very good at reducing the edema (fluids) and eliminating the abnormal blood vessels that characterize wet macular degeneration, but our results suggest that there could be unanticipated side effects.”

Glycemic Control Appears to Reduce Type 1 Diabetics’ Retinopathy Risk; Night Vision Symptoms May Predict Macular Degeneration Progression

2008-11-22T17:20:00.000-08:00

Highlights of the November 2008 issue of “Ophthalmology”

This month’s Ophthalmology, the journal of the American Academy of Ophthalmology, reports on the conclusions from a population-based study of risk factors related to progression or regression of diabetic retinopathy over a 25 year period in people with Type 1 diabetes, and on the associations found between night vision symptoms and progression of age-related macular degeneration (AMD) in a cohort study within the Complications of Age-related Macular Degeneration Prevention Trial (CAPT), a multi-center randomized clinical trial.

Risk Factors for Retinopathy in Persons with Type 1 Diabetes
Many people who have Type 1 or Type 2 diabetes develop retinopathy, a serious disorder that damages the eye’s retina, the area of the back of the eye where images are focused and relayed to the brain’s visual cortex. Ophthalmologists (Eye M.D.s) monitor their diabetic patients for signs of retinopathy and use lifestyle recommendations, medications, and surgical approaches as appropriate to reduce the risk that diabetic retinopathy (DR) will progress to the proliferative stage (PDR), in which abnormal blood vessel growth leads to visual impairment. In recent years the diagnosis, prevention and treatment of DR and PDR have improved markedly.

The Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) is a large, long-term study that confirmed and expanded on results of other significant DR studies such as the Diabetes Control and Complications Trial. Ronald Klein, MD, and colleagues evaluated factors associated with the progression or regression of retinopathy over a 25 year period in people who had been diagnosed with Type 1 diabetes before the age of 30 years. The key finding was that glycemic control--assessed via blood levels of glycosylated hemoglobin A1, a reliable measure of average blood sugar--at the time of the baseline exam and throughout the study was strongly related to whether a patient’s DR worsened or improved. This confirmed findings of a number of earlier large studies. Better glycemic control was associated with significant reduction in DR progression and increased improvement in DR independent of how long the patient had had Type 1 diabetes and the level of DR at the baseline exam. Other risk factors found by the WESDR to be associated with progression to PDR included male gender, higher blood pressure level, presence of protein in urine (a manifestation of diabetic kidney disease) and a greater body mass index as measured at baseline.

WESDR participants were 955 insulin-taking Type 1 diabetics who received baseline exams between 1980 and 1982 and were either evaluated again four years later or died before the four-year follow up. Additional follow up exams were done at 10, 14 and 25 years post-baseline, and 520 of the original participants completed the 25-year follow-up.

Based on WESDR findings, the researchers estimate that over a 25-year period, 185,000 to 466,000 Americans with Type 1 diabetes will develop PDR. Dr. Klein adds the caution that these numbers may be an overestimation, because PDR incidence has declined in people diagnosed with Type 1 diabetes in recent years, possibly due to proactive and improved treatment of glycemia and blood pressure.

What Might Declining Night Vision Mean for AMD Patients?
The Complications of Age-Related Macular Degeneration Prevention Trial (CAPT) Research Group assessed night vision in a cohort of 1,052 CAPT patients. The main purpose of CAPT, a National Eye Institute-sponsored multicenter randomized clinical trial conducted from 1999 to 2005, was to investigate whether low-intensity laser treatment could prevent vision loss in patients with early stage age-related macular degeneration (AMD). In advanced stages, AMD destroys the macula in the eye’s retina, the area that normally provides the detailed, central vision we rely on for reading, driving and other daily tasks. The CAPT results did not show that the laser treatment prevented vision loss, but data from the CAPT cohort did identify a new way to predict AMD progression.

Earlier studies had shown that loss of photoreceptor (light sensitive) cells, particularly “rod” cells involved in night vision, occurs before the disease progresses to advanced AMD in the retina, which indicated that assessing night vision might be a good way to track AMD progression. In the CAPT, patients with signs of early AMD, defined as 10 or more large deposits known as drusen on the retina and vision 20/40 or better, initially completed a 10-item night vision self-assessment questionnaire that rated difficulties with night driving and problems with vision deficits during low-light activities like reading or watching movies. The patients were followed-up annually up to five or six years. Data analyses led by Gui-shuang Ying, PhD, showed that those who had the worst night vision at baseline were the most likely to develop geographic atrophy (GA), or choroidal neovascularization (CNV) and to experience reduced visual acuity. GA is also known as advanced “dry” AMD, and CNV as “wet” AMD.

Since the association of night vision symptoms and AMD progression is clear and the 10-item questionnaire is simple and inexpensive to administer, Dr. Ying concludes that this could be a useful way for ophthalmologists to identify patients at high risk and intervene early to prevent vision loss and the progression to advanced AMD.

Eds: Full texts of the studies are available from the Academy’s media relations department.
About the American Academy of Ophthalmology

AAO is the world's largest association of eye physicians and surgeons—Eye M.D.s—with more than 27,000 members worldwide. Eye health care is provided by the three “O’s” – opticians, optometrists and ophthalmologists. It is the ophthalmologist, or Eye M.D., who can treat it all: eye diseases and injuries, and perform eye surgery. To find an Eye M.D. in your area, visit the Academy's Web site at www.aao.org.

Anti-VEGF Drugs For Retinal Diseases Could Have Serious Side Effects, Scientists Caution

2008-11-22T17:17:00.000-08:00

ScienceDaily (Nov. 5, 2008) — Scientists at Schepens Eye Research Institute have found that reducing the levels of vascular endothelial growth factor (VEGF), which is best known as a stimulator of new blood vessel growth, in adult mice causes the death of photoreceptors and Muller glia - cells of the retina that are essential to visual function.

This finding holds implications for the chronic use of promising new anti-VEGF drugs such as Lucentis, which eliminate abnormal and damaging blood vessel growth and leakage in the retina by neutralizing VEGF.

"The take home message of this study is that physicians should be vigilant in monitoring patients undergoing anti-VEGF treatments for any possible signs of these side effects," says Principal Investigator Patricia D'Amore, Senior Scientist at Schepens Eye Research Institute. "Drugs such as Lucentis are very good at reducing the edema (fluids) and eliminating the abnormal blood vessels that characterize wet macular degeneration, but our results suggest that there could be unanticipated side effects."

Scientists have long known that VEGF is essential for normal development of the vascular system and for wound healing. It triggers the formation of new blood vessels that nourish the growing body and heal organs and tissues. VEGF also stimulates--in an apparent misguided attempt to heal perceived damage in the retina--the growth of abnormal blood vessels that leak and damage delicate retinal tissue.

However, a growing body of evidence also indicates that beyond its impact on blood vessel growth, VEGF may play other vital roles in the adult body and eye, so that eliminating the growth factor might lead to unexpected consequences.

Given the popularity and promise of the new anti-VEGF drugs for the treatment of macular degeneration, D'Amore and her team believed that investigating the broader role of this growth factor in the normal adult retina was critical. She and her laboratory mimicked the action of the anti-VEGF drugs by introducing into adult mice a soluble VEGF receptor, known as sFlt1, which binds and neutralizes the VEGF-- in much the same way that Lucentis does in the eye.

After two weeks, the team found no effect on blood vessels of the inner retina, but did find a significant increase in the number of dying cells of the inner and outer nuclear layers which include amacrine cells that participate in transmitting the visual signal; Muller cells that also participate in the visual signal and support the photoreceptors; and, photoreceptors, which are responsible for color and night vision. The team then used electroretinograms to measure visual function and found a significant loss in visual function. Consistent with these observations, they discovered that both photoreceptors and Muller cells express VEGFR2, the major VEGF signaling receptor and they found that neighboring Muller cells express VEGF.

Parallel studies in tissue culture demonstrated that suppressing VEGF in Muller cells led to Muller cell death, indicating an autocrine role for VEGF in Muller cells (i.e. Muller cells both make VEGF and use it for survival). Further, they used cultures of freshly isolated photoreceptors to show that VEGF can act as a protectant for these cells.

"Insight into the complex role of VEGF in the eye and in other parts of the body indicates that increased care should be taken in the long-term use of these drugs and that this new information should be considered in the design of future clinical studies to ensure that these possible side effects are taken into account," says D'Amore.

"Mice eyes differ from human eyes in many ways, so we cannot directly extrapolate these results to humans, but this study is an important heads-up that clinical application of anti-VEGF therapy in the eye needs to proceed with caution," she adds.

From a clinical perspective, Dr. Delia Sang of Ophthalmic Consultants of Boston points out that the use of anti-VEGF therapy in the treatment of patients with wet macular degeneration has revolutionized outcomes in this disease. However, in light of the work of Dr. D'Amore and others, in elucidating possible systemic and ocular side effects of these drugs, "caution must be exercised in identifying patients at increased risk of problems with long-=term VEGF blockade, and potential side effects must be detected early in the assessment of patients who will require repeated dosages of anti-VEGF agents."

The study is also relevant to the drug Avastin, which was initially approved for intravenous use as an anti-angiogenic agent in the treatment of cancer, but is also widely used intravitreally for the treatment of wet AMD because of its similar mode of action and much lower cost.

The next steps in D'Amore's research will include investigating the specific functions of VEGF in the eye.

This research is published in the November 3, 2008 PLoS ONE. Authors of the study include: Magali Saint-Geniez, Arindel S. R. Maharaj, Tony E. Walshe, Budd A. Tucker, Eiichi Sekiyama, Tomoki Kurihara, Diane C. Darland, Michael J. Young, Patricia A. D'Amore

Adapted from materials provided by Schepens Eye Research Institute, via EurekAlert!, a service of AAAS.

Anti-VEGF Drugs for Retinal Diseases Could Have Serious Side Effects, Scientists Caution

2008-11-22T17:15:00.000-08:00

BOSTON, Nov 03, 2008 /PRNewswire via COMTEX/ -- Scientists at Schepens Eye Research Institute have found that reducing the levels of vascular endothelial growth factor (VEGF), which is best known as a stimulator of new blood vessel growth, in adult mice causes the death of photoreceptors and Muller glia -- cells of the retina that are essential to visual function. This finding, published in the November 3, 2008 PLoS ONE, holds implications for the chronic use of promising new anti-VEGF drugs such as Lucentis, which eliminate abnormal and damaging blood vessel growth and leakage in the retina by neutralizing VEGF.

"The take home message of this study is that physicians should be vigilant in monitoring patients undergoing anti-VEGF treatments for any possible signs of these side effects," says Principal Investigator Patricia D'Amore, Senior Scientist at Schepens Eye Research Institute. "Drugs such as Lucentis are very good at reducing the edema (fluids) and eliminating the abnormal blood vessels that characterize wet macular degeneration, but our results suggest that there could be unanticipated side effects."

Scientists have long known that VEGF is essential for normal development of the vascular system and for wound healing. It triggers the formation of new blood vessels that nourish the growing body and heal organs and tissues. VEGF also stimulates -- in an apparent misguided attempt to heal perceived damage in the retina -- the growth of abnormal blood vessels that leak and damage delicate retinal tissue.

However, a growing body of evidence also indicates that beyond its impact on blood vessel growth, VEGF may play other vital roles in the adult body and eye, so that eliminating the growth factor might lead to unexpected consequences.

Given the popularity and promise of the new anti-VEGF drugs for the treatment of macular degeneration, D'Amore and her team believed that investigating the broader role of this growth factor in the normal adult retina was critical. She and her laboratory mimicked the action of the anti-VEGF drugs by introducing into adult mice a soluble VEGF receptor, known as sFlt1, which binds and neutralizes the VEGF -- in much the same way that Lucentis does in the eye.

After two weeks, the team found no effect on blood vessels of the inner retina, but did find a significant increase in the number of dying cells of the inner and outer nuclear layers which include amacrine cells that participate in transmitting the visual signal; Muller cells that also participate in the visual signal and support the photoreceptors; and, photoreceptors, which are responsible for color and night vision. The team then used electroretinograms to measure visual function and found a significant loss in visual function. Consistent with these observations, they discovered that both photoreceptors and Muller cells express VEGFR2, the major VEGF signaling receptor and they found that neighboring Muller cells express VEGF.

Parallel studies in tissue culture demonstrated that suppressing VEGF in Muller cells led to Muller cell death, indicating an autocrine role for VEGF in Muller cells (i.e. Muller cells both make VEGF and use it for survival). Further, they used cultures of freshly isolated photoreceptors to show that VEGF can act as a protectant for these cells.

"Insight into the complex role of VEGF in the eye and in other parts of the body indicates that increased care should be taken in the long-term use of these drugs and that this new information should be considered in the design of future clinical studies to ensure that these possible side effects are taken into account," says D'Amore.

"Mice eyes differ from human eyes in many ways, so we cannot directly extrapolate these results to humans, but this study is an important heads-up that clinical application of anti-VEGF therapy in the eye needs to proceed with caution," she adds.

From a clinical perspective, Dr. Delia Sang of Ophthalmic Consultants of Boston points out that the use of anti-VEGF therapy in the treatment of patients with wet macular degeneration has revolutionized outcomes in this disease. However, in light of the work of Dr. D'Amore and others, in elucidating possible systemic and ocular side effects of these drugs, "caution must be exercised in identifying patients at increased risk of problems with long-term VEGF blockade, and potential side effects must be detected early in the assessment of patients who will require repeated dosages of anti-VEGF agents."

The study is also relevant to the drug Avastin, which was initially approved for intravenous use as an anti-angiogenic agent in the treatment of cancer, but is also widely used intravitreally for the treatment of wet AMD because of its similar mode of action and much lower cost.

The next steps in D'Amore's research will include investigating the specific functions of VEGF in the eye.

Authors of the study include: Magali Saint-Geniez (1,2), Arindel S. R. Maharaj (1), Tony E. Walshe (1,2), Budd A. Tucker (1,2), Eiichi Sekiyama (1,2), Tomoki Kurihara (1), Diane C. Darland (4), Michael J. Young (1,2), Patricia A. D'Amore (1,2,3)
(1) Schepens Eye Research Institute
(2) Department of Ophthalmology, Harvard Medical School
(3) Department of Pathology, Harvard Medical School
(4) University of North Dakota, Grand Forks, North Dakota

Ten Years of Data on Studies of Age-Related Eye Disease Now Available to Researchers

2008-11-22T17:12:00.000-08:00

Looked at progression of age-related macular degeneration and age-related cataract in 4,757 older adults

Nov. 11, 2008 - Ten years of data collected during the Age-Related Eye Disease Study (AREDS), which looked at the progression of age-related macular degeneration and age-related cataract, has been released by the National Eye Institute (NEI). Researchers can apply for access to this complete set of medical history records and clinical trial results, as well as select genetic information to gain a better understanding of two complicated vision conditions that affect aging adults.

"This vast pool of data is now at the fingertips of scientists, which is an unprecedented occurrence in the field of ophthalmology," said Frederick L. Ferris III, M.D., clinical director of the NEI, which is, part of the National Institutes of Health (NIH).

"Now that the entire AREDS database is available to the global research community, we hope that researchers will be inspired to delve more deeply into analyzing the genetic and environmental factors involved in the onset and progression of age-related macular degeneration and age-related cataract."

The AREDS data are accessible through the online database of Genotypes and Phenotypes, known as dbGaP, which archives and distributes data from studies that explore the relationships between genetic variations (genotypes) and observable traits (phenotypes).

The NEI-supported AREDS was one of two studies included in the December 2006 launch of dbGaP. The National Library of MedicineÅfs National Center for Biotechnology Information (NCBI) created and operates dbGaP, which includes two levels of access.

>> Study descriptions and documents such as protocols can be found in the public, open-access section.

>> In the controlled-access section, approved researchers can view genotype and phenotype data from individual AREDS participants, though the information is coded to protect patientsÅf identities.

The first version of controlled-access AREDS data became available through dbGaP in June 2007. It included selected phenotypic data and information gathered from a genome-wide scan of DNA samples collected from 600 AREDS participants.

The updated version now incorporates the complete information obtained from all 4,757 AREDS participants during trial enrollment and follow-up visits, including data from photographs of the patients' eyes and information regarding their nutritional intake, quality of life, and rates of illness and death.

"Providing this new set of AREDS data through dbGaP will benefit researchers worldwide who are investigating genetic factors in age-related macular degeneration and other conditions," said David Lipman, M.D., director of the NCBI.

"AREDS was one of two founding studies in dbGaP, and its availability over the last year and a half has enabled many research teams to conduct their own analyses of these important data. We are delighted to have received, and to make available, this even more extensive set of data, further enhancing the possibilities for research and discovery."

AREDS began in 1992 as a long-term, multi-center, prospective study designed to evaluate the progression of age-related macular degeneration and age-related cataract. Participants were also enrolled in a clinical trial of high-dose vitamin and mineral supplements. They were followed for a median of 6.5 years during the trial and an additional five years after the trial's conclusion.

In addition, DNA was isolated from blood samples taken from more than 3,700 AREDS participants beginning in 1998. DNA from many of these participants is currently being stored in the NEI-AREDS Genetic Repository. Access to these DNA samples for research purposes is available for a fee through the Coriell Institute for Medical Research at http://ccr.coriell.org/Sections/Collections/AREDS/?SsId=68.

"Genetic testing has become crucial in the advancement of science, both for understanding the progression of diseases and for determining appropriate research directions for treatments," said Paul A. Sieving, M.D., Ph.D., director of the NEI. "With the AREDS data available through dbGaP, vision researchers can continue to identify genetic factors that may play a role in eye conditions such as age-related macular degeneration and cataract."

The public, open-access AREDS data can be viewed on the dbGaP website at http://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000001.v2.p1. Researchers can find a link to the application for controlled access to individual-level data on the same site.

More information about AREDS (NCT00000145) can be found at www.clinicaltrials.gov.

The National Eye Institute (NEI), a component of the National Institutes of Health, is the federal government's lead agency for vision research that leads to sight-saving treatments and plays a key role in reducing visual impairment and blindness. For more information, visit the NEI Web site at www.nei.nih.gov.

The National Center for Biotechnology Information (NCBI) was established in 1988 as a national resource for molecular biology information. NCBI creates public databases, conducts research in computational biology, develops software tools for analyzing molecular and genomic data, and disseminates biomedical information, all for the better understanding of processes affecting human health and disease. NCBI is a division of the National Library of Medicine, the world's largest library of the health sciences. For more information, visit www.nlm.nih.gov.

The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

Retinal Imaging: The Future is Bright with New Technologies

2008-11-22T17:08:00.000-08:00

By John W. Kitchens, MD

Introduction
There have been certain major “eras” in ophthalmology. These could include: the phaco era, the refractive era, the anti-VEGF era, among others. I believe we are about to enter into “the imaging era”, specifically in regard to the management of retinal diseases. At no time in the history of ophthalmology have more companies come forth to develop and market the same technology as spectral domain OCT. Although this technology is exciting and is taking “center stage”, other interesting imaging techniques are beginning to develop.

Autofluorescence utilization is becoming more and more common and the information that it yields may play an important role by improving our understanding of AMD and other hereditary retinal disorders. The technology that forms the foundation of autofluorescence has improved rapidly in the last few years and this imaging modality is about to enter “prime time” in the retina world.

Ultrawide angle imaging is another exciting technology that may have retina specialists rethinking some of their understanding and approaches to retinal vascular diseases (e.g, diabetic retinopathy, vascular occlusions, etc), uveitis, and heritable retinal diseases. It is a revolutionary system that can improve our understanding of many common retinal diseases. In this article, I hope to provide a brief overview to some of the technologies that may develop alongside spectral domain OCT.

Autofluorescence (AF)
Although fundus autofluorescence has received particular attention recently, it has actually been around for some time.. Autofluorescence was initially described prior to initiating the dye injection in fluorescein angiography. At that time, it was described as “pseudofluorescence” [1]. With the advent of the confocal scanning laser ophthalmascope (cSLO) [2,3], autofluorescence has become much more functional as a tool for evaluating the health of the RPE (among other things). Autofluorescence can also be performed with a standard fundus camera incorporating special filters [4]. Images obtained using this technique are of lower quality due to the presence of naturally occurring fluorophores in the lens and other structures of the eye. Also, because of the low levels of illumination created by autofluorescence, multiple images (usually 4-16) are obtained and are averaged with normalized pixel values represented in the final image.

Autofluorescence of the fundus is primarily due to the presence of lipofuscin (along with other fluorophores) in the RPE. Lipofuscin accumulates in aging RPE cells and represents the incomplete degradation of photoreceptor outer segments [5]. Increased autofluorescence can be seen with RPE dysfunction representing a decreased ability of the RPE to metabolize or eliminate the byproducts of phototransduction. Decreased autofluorescence occurs with the loss of photoreceptor outer segments. Hence autofluorescence can give information regarding the health of the RPE and outer retina in various disorders.

Autofluorescence adds insight into various disease states. Diseases characterized by the accumulation of fluorophores (Best disease and Stargardt’d disease) shows characteristically intense autofluorescence [6.7]. Autofluorescent findings may also help to explain the lack of visual recovery in some cases of central serous chorioretinopathy [8]. AMD demonstrates autofluorescent findings that can predict progression of geographic atrophy [9], as well as help characterize drusen and pigment epithelial detachments. Most interesting in “wet” AMD is the use of autofluorescent characteristics as a possible predictor of visual acuity improvement with the use of anti-VEGF therapy [10].

Currently, the only cSLO-based system available for obtaining autofluorescent images is the Heidelberg Retina Angiograph (the HRA classic, HRA 2, and Spectralis HRA; Heidelberg Engineering, Heidelberg, Germany). The Spectralis is a unique device that is essentially the “Swiss Army Knife” of retinal imaging. This device has the ability to perform 6 different imaging modalities including: fluorescein angiography, ICG, autofluorescence, high speed/resolution OCT, red-free, and infrared imaging. Not only can the Spectralis perform all of these different imaging modalities (some at the same time), but it creates a reference point for location and correction of these various images to ensure that the same points are being imaged from visit to visit. It should also be noted that cSLO instuments from both Rodenstock (Rodenstock, Weco, Dusseldorf, Germany) and Zeiss (Zeiss, Oberkochen, Germany) are in development.

Ultrawide Angle Imaging
Fluorescein angiography has been fundamental to the understanding of vascular disorders affecting the retina and choroid. Since it was first described in 1961 [11], arguably, no diagnostic procedure has led to a better understanding of diseases that affect the posterior pole than angiography. From A-to-Z (or AMD to AZOOR), fluorescein angiography was essential in our understanding of the most common and the rarest of retinal disorders. Since its inception, fluorescein angiography has undergone incremental improvements in camera systems, image processing, and the transition to digital angiography. The gradual evolution in angiography has led to higher quality images in a more patient-friendly (quicker) method.

The next step in this evolution is that of ultrawide angle angiography. The Optos P200A (Optos Inc., Dunfermline, Scotland) is the first noncontact system that offers up to a 200 degree view of the retina in a single image. I have had the opportunity to utilize this system over the last 6 months and must admit that it has changed my approach to many retinal diseases. In no disease was imaging of the retinal periphery more valuable than diabetic retinopathy.

Initially, I began obtaining ultrawide angle angiography in patients with proliferative diabetic retinopathy. My intent was to identify the area of neovascularization (NVE) and degree of nonperfusion in patients presenting with mild vitreous hemorrhage. While imaging these (affected) eyes, I was astounded to see that, often, the fellow (asymptomatic) eye had more profound changes than the eye with hemorrhage. This is particularly important in diabetic patients due to the fact that a hemorrhage in their fellow eye would leave them unable to drive, dose their insulin, and perform other vital activities of daily living. These findings led me to perform earlier panretinal laser in the fellow eye in an effort to “head-off” any problems that may develop.

Patients with clinically significant diabetic macular edema also demonstrated a wide variety of peripheral findings on ultrawide angle angiography. These findings ranged from excellent peripheral perfusion to extreme nonperfusion. The cases with extensive nonperfusion seemed (in my clinical observation) to respond more favorably to intravitreal Avastin (bevacizumab). This association has been described by others (primarily Steve Schwartz, MD and his colleagues at UCLA) with access to the Optos system.

This is an exciting time to practice retina. Improvements such as anti-VEGF therapy and small gauge surgery have made retina a great area to specialize in. These new technologies in retinal imaging will continue to add to this excitement and will help our understanding of various retinal conditions. This understanding will lead to better treatments and outcomes.

References
1. Machemer, R., et al. Pseudofluorescence--a problem in interpretation of fluorescein angiograms. Am J Ophthalmol. 1970: 70(1); 1-10.
2. von Ruckmann, A., F.W. Fitzke, and A.C. Bird. Distribution of fundus autofluorescence with a scanning laser ophthalmoscope. Br J Ophthalmol. 1995: 79(5); 407-412.
3. Delori, F.C., et al. In vivo fluorescence of the ocular fundus exhibits retinal pigment epithelium lipofuscin characteristics. Invest Ophthalmol Vis Sci. 1995. 36(3): 718-729.
4. Spaide, R.F. Fundus autofluorescence and age-related macular degeneration. Ophthalmology. 2003. 110(2): 392-399.
5. Feeney-Burns, L., E.R. Berman, and H. Rothman. Lipofuscin of human retinal pigment epithelium. Am J Ophthalmol. 1980. 90(6): 783-791.
6. Jarc-Vidmar, M., A. Kraut, and M. Hawlina. Fundus autofluorescence imaging in Best's vitelliform dystrophy. Klin Monatsbl Augenheilkd. 2003. 220(12): 861-867.
7. Lois, N., et al. Fundus autofluorescence in Stargardt macular dystrophy-fundus flavimaculatus. Am J Ophthalmol. 2004. 138(1): 55-63.
8. Framme, C., et al., Fundus autofluorescence in acute and chronic-recurrent central serous chorioretinopathy. Acta Ophthalmol Scand. 2005. 83(2): 161-167.
9. Schmitz-Valckenberg, S., et al. Correlation between the area of increased autofluorescence surrounding geographic atrophy and disease progression in patients with AMD. Invest Ophthalmol Vis Sci, 2006. 47(6): 2648-2654.
10. Heimes, B., et al., Foveal RPE autofluorescence as a prognostic factor for anti-VEGF therapy in exudative AMD. Graefes Arch Clin Exp Ophthalmol. 2008. 246(9): 1229-1234.
11. Novotny, H.R. and D.L. Alvis, A method of photographing fluorescence in circulating blood in the human retina. Circulation. 1961. 24: 82-86.

Implantable Telescope for End-Stage Age-related Macular Degeneration: Long-term Visual Acuity and Safety Outcomes

2008-11-22T17:07:00.000-08:00

R. Doyle Stultingb, Jeffrey S. Heierc, Stephen S. Laned, David F. Change, Lawrence J. Singermanf, Cynthia A. Bradfordg, Robert E. Leonardg, IMT002 Study Group

Purpose
To evaluate long-term safety and best-corrected visual acuity (BCVA) results of a telescope prosthesis in patients with end-stage age-related macular degeneration (AMD).

Design
Prospective, open-label clinical trial with fellow-eye controls.

Methods
Patients with end-stage AMD (bilateral geographic atrophy or disciform scars; BCVA, 20/80 to 20/800) received the telescope prosthesis at 28 centers. Methods were similar to those described in the one-year results, with follow-up visits continuing at 18 and 24 months. Main outcome measures included BCVA change from baseline, endothelial cell density (ECD) and morphometry, and incidence of complications.

Results
At two years, data from 174 (92.6%) of 188 available patients were analyzed. Overall, 103 (59.5%) of 173 telescope-implanted eyes gained three lines or more (doubling of visual angle) of BCVA compared with 18 (10.3%) of 174 fellow control eyes (P < .0001). Mean BCVA improved 3.6 lines (standard deviation [SD], 1.9 lines) and 2.8 lines (SD, 2.3 lines) from baseline in eyes with the 3X and 2.2X device models, respectively. Mean ECD stabilized through two years, with 2.4% mean cell loss occurring from one to two years. There was no significant change in coefficient of variation or percentage of hexagonal endothelial cells from within six months to two years after surgery. The most common complication was inflammatory deposits.

Conclusions
Long-term results of this telescope prosthesis show the substantial BCVA improvement at one year is maintained at two years. Key indicators of corneal health demonstrate ECD change that reflects remodeling of the endothelium associated with the implantation procedure. ECD stabilizes over time, and there is no evidence of any ongoing endothelial trauma.

Brain Reorganizes To Adjust For Loss Of Vision

2008-11-22T13:28:00.001-08:00

ScienceDaily (Nov. 21, 2008) — A new study from Georgia Tech shows that when patients with macular degeneration focus on using another part of their retina to compensate for their loss of central vision, their brain seems to compensate by reorganizing its neural connections. Age–related macular degeneration is the leading cause of blindness in the elderly. The study appears in the December edition of the journal Restorative Neurology and Neuroscience.

“Our results show that the patient’s behavior may be critical to get the brain to reorganize in response to disease,” said Eric Schumacher, assistant professor in Georgia Tech’s School of Psychology. “It’s not enough to lose input to a brain region for that region to reorganize; the change in the patient’s behavior also matters.”

In this case, that change of behavior comes when patients with macular degeneration, a disease in which damage to the retina causes patients to lose their vision in the center of their visual field, make up for this loss by focusing with other parts of their visual field.

Previous research in this area showed conflicting results. Some studies suggested that the primary visual cortex, the first part of the cortex to receive visual information from the eyes, reorganizes itself, but other studies suggested that this didn’t occur. Schumacher and his graduate student, Keith Main, worked with researchers from the Georgia Tech/Emory Wallace H. Coulter Department of Biomedical Engineering and the Emory Eye Center. They tested whether the patients’ use of other areas outside their central visual field, known as preferred retinal locations, to compensate for their damaged retinas drives, or is related to, this reorganization in the visual cortex.

The researchers presented 13 volunteers with a series of tests designed to visually stimulate their peripheral regions and measure brain activity with functional magnetic resonance imaging. They found that when patients visually stimulated the preferred retinal locations, they increased brain activity in the same parts of the visual cortex that are normally activated when healthy patients focused on objects in their central visual field. They concluded that the brain had reorganized itself.

The parts of the visual cortex that process information from the central visual field in patients with normal vision were reprogrammed to process information from other parts of the eye, parts that macular degeneration patients use instead of their central visual areas.

While there is evidence with other tasks that suggests that the brain can reorganize itself, this is the first study to directly show that this reorganization in patients with retinal disease is related to patient behavior.

The research group is currently studying how long this reorganization takes and whether it can be fostered through low-vision training.

The research was funded in part by a seed grant from the Georgia Tech/Emory Health Systems Institute.

Study Shows Lutein and Zeaxanthin Protect Against Age-Related Macular Degeneration

2008-11-22T13:25:00.000-08:00

(NaturalNews) Researchers from Ohio State University may have discovered a mechanism by which proteins known as xanthophylls help prevent against age-related vision loss, they reported in a study published in the Journal of Lipid Research.

"Our research to understand this mechanism might provide a greater appreciation for how one could intervene to possibly slow macular degeneration," said senior study author Earl Harrison.

Age-related macular degeneration is one of the most common causes of age-related vision loss and affects approximately 10 million people in the United States. The deterioration of the macula, a tissue located in the center of the retina, causes vision in the center of the eye to blur, which lead to functional blindness. The condition cannot be reversed once it develops; it can only be slowed.

Prior research has suggested that the xanthophyll proteins lutein and zeaxanthin may protect against the eight-related macular degeneration by filtering out potentially harmful light from the blue end of the spectrum and also protecting the eye against damage from oxidation. The two proteins have been observed to concentrate in the macula, forming a yellow spot.

In the current study, researchers tested the hypothesis that the xanthophylls are transported to the macula by proteins known as scavenger receptor class B, type 1 (SR-B1). They treated pigment cells from the lining of the human retina with lutein, zeaxanthin and the related compounds beta-carotene, finding that the cells absorbed more xanthophylls than they did beta-carotene.

The researchers then blocked the action of SR-B1 by one of two methods. Both of the methods led to a decrease in xanthophyll of distortion of 41 to 87 percent.

Lutein and zeaxanthin cannot be synthesized by the body, but must be consumed in foods such as green, leafy vegetables, peas, summer squash, or yellow and orange fruits and vegetables (including carrots, papaya and peaches).