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.
Saturday, October 23, 2010
Monday, October 18, 2010
Vitamin A pill could save sight
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.’
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.
More...
* The age of the pensionista: Why most women are totally unprepared for retirement
* The rise of the silver surfer: How half of women over 55 log on to Facebook
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.’
Sunday, October 10, 2010
Prizes Honor Studies in Vision Loss
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.
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.
Monday, October 4, 2010
Portable Macular Degeneration (AMD) Early Detection & Screening Device
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.
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.
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