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.
Wednesday, June 2, 2010
Thursday, May 27, 2010
Decreased antioxidant levels increase risk of age-related macular degeneration with exposure to sunlight
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.
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.
Friday, January 22, 2010
Promising new treatment for dry AMD in clinical trials
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
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
Sunday, January 10, 2010
Laureate Pharma and Iconic Therapeutics complete manufacturing hI-con1 recombinant Fc-Factor VII fusion protein
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
"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
Monday, January 4, 2010
New research findings may help stop age-related macular degeneration at the molecular level
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
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
Monday, December 14, 2009
Scripps Research scientists crack mystery of protein's dual function
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
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
Thursday, December 3, 2009
Save your eyesight – stop smoking!
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
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
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