Jan. 25, 2013 — Doctors may one day treat some forms of blindness by altering the genetic program of the light-sensing cells of the eye, according to scientists at Washington University School of Medicine in St. Louis.

Working in mice with retinitis pigmentosa, a disease that causes gradual blindness, the researchers reprogrammed the cells in the eye that enable night vision. The change made the cells more similar to other cells that provide sight during daylight hours and prevented degeneration of the retina, the light-sensing structure in the back of the eye. The scientists now are conducting additional tests to confirm that the mice can still see.

“We think it may be significantly easier to preserve vision by modifying existing cells in the eye than it would be to introduce new stem cells,” says senior author Joseph Corbo, MD, PhD, assistant professor of pathology and immunology. “A diseased retina is not a hospitable environment for transplanting stem cells.”

The study is available in the early online edition of Proceedings of the National Academy of Sciences.

Mutations in more than 200 genes have been linked to various forms of blindness. Efforts are underway to develop gene therapies for some of these conditions.

Rather than seek treatments tailored to individual mutations, Corbo hopes to develop therapies that can alleviate many forms of visual impairment. To make that possible, he studies the genetic factors that allow cells in the developing eye to take on the specialized roles necessary for vision.

The retina has two types of light-sensing cells or photoreceptors. The rods provide night vision, and the cones sense light in the daytime and detect fine visual details.

In retinitis pigmentosa, the rods die first, leaving patients unable to see at night. Daytime vision often remains intact for some time until the cones also die.

Corbo and others have identified several genes that are active in rods or in cones but not in both types of photoreceptors. He wondered whether turning off a key gene that is activated only in rods could protect the cells from the loss of vision characteristic of retinitis pigmentosa.

‘”The question was, when retinitis pigmentosa is caused by a mutation in a protein only active in rods, can we reduce or stop vision loss by making the cells less rod-like?” he explains.

The new study focuses on a protein known as Nrl, which influences development of photoreceptors. Cells that make Nrl become rods, while cells that lack the protein become cones. Turning off the Nrl gene in developing mice leads to a retina packed with cone cells.

To see if this rod-to-cone change was possible in adult mice, Corbo created a mouse model of retinitis pigmentosa with an Nrl gene that could be switched on and off by scientists.

“In adult mice, switching off Nrl partially converts the rod cells into cone cells,” he says. “Several months later, when the mutant mice normally had very little vision left, we tested the function of their retina.”

The test showed a healthier level of electrical activity in the retinas of mice that lacked Nrl, suggesting that the mice could still see.

Corbo now is looking for other critical development factors that can help scientists more fully transform adult rods into cones. He notes that if complete conversion of rods to cones were possible, this therapy could also be helpful for conditions where cone cells die first, such as macular degeneration.

Montana CL, Kolesnikov AV, Shen SQ, Myers CA, Kefalov VJ, Corbo JC. Reprogramming of adult rod photoreceptors prevents retinal degeneration. Proceedings of the National Academy of Sciences, online January 14, 2013.

Funding from the National Eye Institute (EY018826 and EY019312), an Institutional Vision Science Training Grant (EY13360) and a grant from Research to Prevent Blindness to the Department of Ophthalmology and Visual Sciences at Washington University supported this research.​

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The above story is reprinted from materials provided by Washington University in St. Louis. The original article was written by Michael C. Purdy.

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Journal Reference:

1. C. L. Montana, A. V. Kolesnikov, S. Q. Shen, C. A. Myers, V. J. Kefalov, J. C. Corbo. Reprogramming of adult rod photoreceptors prevents retinal degeneration. Proceedings of the National Academy of Sciences, 2013; DOI: 10.1073/pnas.1214387110

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Jan. 21, 2013 — Independent clinical trials, including one conducted at the Scheie Eye Institute at the Perelman School of Medicine, have reported safety and efficacy for Leber congenital amaurosis (LCA), a congenital form of blindness caused by mutations in a gene (RPE65) required for recycling vitamin A in the retina. Inherited retinal degenerative diseases were previously considered untreatable and incurable. There were early improvements in vision observed in the trials, but a key question about the long-term efficacy of gene therapy for curing the retinal degeneration in LCA has remained unanswered.

Now, new research from the Scheie Eye Institute, published this week in the Proceedings of the National Academy of Sciences, finds that gene therapy for LCA shows enduring improvement in vision but also advancing degeneration of affected retinal cells, both in LCA patients and animal models of the same condition.

LCA disease from RPE65 mutations has two-components: a biochemical blockade leading to impaired vision, and a progressive loss of the light-sensing photoreceptor cells throughout life of the affected patient. The authors of the new study explain that until now gene therapy has been optimistically assumed, but not proven, to solve both disease components at the same time.

“We all hoped that the gene injections cured both components — re-establishing the cycle of vision and also preventing further loss of cells to the second disease component” said Artur V. Cideciyan, PhD, lead author and co-investigator of an LCA clinical trial at Penn.

Yet, when the otherwise invisible cell layers of the retina were measured by optical imaging in clinical trial participants serially over many years, the rate of cell loss was the same in treated and untreated regions. “In other words, gene therapy improved vision but did not slow or halt the progression of cell loss,” commented Cideciyan.

“These unexpected observations should help to advance the current treatment by making it better and longer lasting,” commented co-author Samuel G. Jacobson, MD, PhD, principal investigator of the clinical trial. “Slowing cell loss in different retinal degenerations has been a major research direction long before the current gene therapy trials. Now, the two directions must converge to ensure the longevity of the beneficial visual effects in this form of LCA.”

In a continuation of the longstanding collaboration between the Scheie investigators and the Section of Ophthalmology at Penn School of Veterinary Medicine headed by co-authors Gustavo D. Aguirre, VMD, PhD, and William A. Beltran, DVM, PhD, studies were performed to test whether the clinical results were also present in the canine model of this LCA at disease stages equivalent to those in human patients.

“Our gene treatment in this canine model provided the groundwork for the clinical trials of patients, and now we added data to confirm the fact that retinal degeneration does continue despite improved vision” said Aguirre. “The next step is to perform the relevant experiments to ask what intervention will stop the degeneration if added to the gene therapy.”

“These new findings contribute to greater clarity in understanding the natural history and complexity of the RPE65 form of LCA and provide a firm foundation for future investigations,” said Joan M. O’Brien MD, professor and chair of the Department of Ophthalmology and director of the Scheie Eye Institute.

Co-authors, in addition to the Penn researchers include, William W. Hauswirth, PhD, professor of Ophthalmology, at the University of Florida, Gainesville.

The current patient studies and the experimental studies were supported by the National Eye Institute (NEI) grants U10 EY017280, EY 06855, 017549, 019304, and 022012, the Macula Vision Research Foundation, and the Foundation Fighting Blindness.

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Jan. 15, 2013 — Scientists at Singapore Eye Research Institute and A*STAR’s Genome Institute of Singapore have succeeded in identifying genes for central corneal thickness that may cause potentially blinding eye conditions. These eye conditions include glaucoma, as well as the progressive thinning of the cornea, which may eventually lead to a need for corneal transplantation.

The authors jointly led a multi-centre study involving 55 hospitals and research centres around the world. They performed a meta-analysis on more than 20,000 individuals in European and Asian populations. Their findings were published in the science journal, Nature Genetics (6 January, 2013).

Central corneal thickness (CCT) is associated with potentially blinding eye conditions such as keratoconus, a condition where the cornea progressively thins and takes on a more conical shape that may eventually require transplantation. CCT has an estimated heritability up to 95% and may determine the severity of one’s glaucoma and assist eye doctors in identifying patients with high risk for progression. In fact, it is one of the leading causes of corneal transplantation worldwide.

The Singapore team has had remarkable success identifying the most CCT-associated loci to date prior to this collaborative world-wide effort, by identifying 6 distinct genetic loci in two papers published in 2011 and 2012 via sample collections involving Singaporean Chinese, Indians, and Malays, as well as Beijing Chinese. However, none was found to be associated with common eye diseases like this study has now shown. Overall this new study identified a total of 27 associated loci, including 6 for the keratoconus.

These observations suggest that most of the CCT-associated loci identified from populations of European descent are shared with Asian populations. These findings show that Singapore is well placed globally in eye and genetics research in finding causes for sight threatening conditions. Eye doctors can in the future through genetic analysis better manage such patients, preventing regression of their conditions.

Prof Aung Tin, Deputy Director, Singapore Eye Research Institute (SERI) and a senior consultant ophthalmologist and Head of Glaucoma Service at Singapore National Eye Centre and a co-author of the paper, said, “This was a tremendous achievement, involving many centres from several countries around the world. Singapore played a major role in this work, especially SERI’s population based studies of 10,000 Chinese, Malay and Indian people.”

Assoc Prof Eranga Vithana, Associate Director, Basic and Experimental Sciences, SERI and a co-author of the paper, said, “This paper identified 6 novel genetic variants that confer increased risk of keratoconus, a condition for which genes were not very forthcoming prior to this study. It once again underlined the inevitability of large scale collaborative studies to unravel genes for common complex diseases and also the advantage of having well characterized large cohorts.”

Assistant Professor Khor Chiea Chuen, Principal Investigator, Division of Human Genetics, Genome Institute of Singapore-an institute of the Agency for Science, Technology and Research (A*STAR) and the paper’s co-lead author, said, “Yet again, this paper underscores the power of modern genetic approaches studied in very large sample sizes in revealing the hereditable basis of normal human traits, and how the extremes of which may give rise to common diseases.”

Prof Ng Huck Hui, Executive Director of the Genome Institute of Singapore said, “I am very pleased that the Genome Institute of Singapore is a part of an international effort to dissect the genetics of eye conditions such as keratoconus and glaucoma. Genomics remains a very powerful tool to identify the link between genetic variations and phenotypes. This study that focuses on central corneal thickness illustrates the value of large scale genetics studies in identifying potential pathways that underlie specific human phenotypes.”

Prof Wong Tien Yin, Executive Director of SERI and Chair, Dept of Ophthalmology, National University Health System (NUHS) and the paper’s senior corresponding author said, “The investment of SERI in population-based studies over the past decade is now paying off with major discoveries in the causes of common eye diseases. This is a team effort and included more than 50 over clinicians, clinician-scientists, research scientists, research staff, statisticians and most importantly, our patients, who have contributed to the collection of these samples.” Adjunct Assoc Prof Jodhbir S Mehta, Head and Senior Consultant, Cornea Service at Singapore National Eye Centre said, “This is a great achievement in collaborative research and offers new insights into keratoconus.”

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The above story is reprinted from materials provided by Agency for Science, Technology and Research (A*STAR), Singapore.

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Journal Reference:

1. Yi Lu, Veronique Vitart, Kathryn P Burdon, Chiea Chuen Khor, Yelena Bykhovskaya, Alireza Mirshahi, Alex W Hewitt, Demelza Koehn, Pirro G Hysi, Wishal D Ramdas, Tanja Zeller, Eranga N Vithana, Belinda K Cornes, Wan-Ting Tay, E Shyong Tai, Ching-Yu Cheng, Jianjun Liu, Jia-Nee Foo, Seang Mei Saw, Gudmar Thorleifsson, Kari Stefansson, David P Dimasi, Richard A Mills, Jenny Mountain, Wei Ang, René Hoehn, Virginie J M Verhoeven, Franz Grus, Roger Wolfs, Raphaële Castagne, Karl J Lackner, Henriët Springelkamp, Jian Yang, Fridbert Jonasson, Dexter Y L Leung, Li J Chen, Clement C Y Tham, Igor Rudan, Zoran Vatavuk, Caroline Hayward, Jane Gibson, Angela J Cree, Alex MacLeod, Sarah Ennis, Ozren Polasek, Harry Campbell, James F Wilson, Ananth C Viswanathan, Brian Fleck, Xiaohui Li, David Siscovick, Kent D Taylor, Jerome I Rotter, Seyhan Yazar, Megan Ulmer, Jun Li, Brian L Yaspan, Ayse B Ozel, Julia E Richards, Sayoko E Moroi, Jonathan L Haines, Jae H Kang, Louis R Pasquale, R Rand Allingham, Allison Ashley-Koch, Paul Mitchell, Jie Jin Wang, Alan F Wright, Craig Pennell, Timothy D Spector, Terri L Young, Caroline C W Klaver, Nicholas G Martin, Grant W Montgomery, Michael G Anderson, Tin Aung, Colin E Willoughby, Janey L Wiggs, Chi P Pang, Unnur Thorsteinsdottir, Andrew J Lotery, Christopher J Hammond, Cornelia M van Duijn, Michael A Hauser, Yaron S Rabinowitz, Norbert Pfeiffer, David A Mackey, Jamie E Craig, Stuart Macgregor, Tien Y Wong. Genome-wide association analyses identify multiple loci associated with central corneal thickness and keratoconus. Nature Genetics, 2013; DOI: 10.1038/ng.2506

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Jan. 16, 2013 — New research in Nature concludes the eye — which depends on light to see — also needs light to develop normally during pregnancy.

Scientists say the unexpected finding offers a new basic understanding of fetal eye development and ocular diseases caused by vascular disorders — in particular one called retinopathy of prematurity that can blind premature infants. The research, led by scientists at Cincinnati Children’s Hospital Medical Center and the University of California, San Francisco (UCSF), appears online Jan. 16 ahead of print publication.

“This fundamentally changes our understanding of how the retina develops,” says study co-author Richard Lang, PhD, a researcher in the Division of Pediatric Ophthalmology at Cincinnati Children’s Hospital Medical Center. “We have identified a light-response pathway that controls the number of retinal neurons. This has downstream effects on developing vasculature in the eye and is important because several major eye diseases are vascular diseases.”

Lang is a principal investigator on the ongoing research along with project collaborator, David Copenhagen, PhD, a scientist in the departments of Ophthalmology and Physiology at UCSF. The scientists say their current study, conducted in mouse models, includes several unexpected findings.

“Several stages of mouse eye development occur after birth,” says Copenhagen. “Because of this, we had always assumed that if light played a role in the development of the eye, it would also happen only after birth.”

But researchers in the current study found that activation of the newly described light-response pathway must happen during pregnancy to activate the carefully choreographed program that produces a healthy eye. Specifically, they say it is important for a sufficient number of photons to enter the mother’s body by late gestation, or about 16 days into a mouse pregnancy.

Researchers were also surprised to learn that photons of light activate a protein called melanopsin directly in the fetus — not the mother — to help initiate normal development of blood vessels and retinal neurons in the eye.

One purpose of the light-response pathway is to suppress the number of blood vessels that form in the retina. These vessels are critical to retinal neurons, which require large amounts of oxygen to form and to function. When retinopathy of prematurity occurs in infants, retinal vessels grow almost unchecked. This continued expansion puts intense pressure on the developing eye and in extreme cases causes severe damage and blindness.

The research team led by Lang and Copenhagen conducted several experiments in laboratory mouse models that allowed them to identify the light-response pathway’s specific components and function.

Mice were reared in the dark and in a normal day-night cycle beginning at late gestation to observe the comparative effects on vascular development of the eye. The researchers verified the function of the light response pathway by mutating an opsin gene in mice called Opn4 that produces melanopsin, in essence preventing activation of the photo pigment.

Both mice reared under dark conditions from late gestation, and those with mutated Opn4, exhibited nearly identical promiscuous expansion of hyaloid vessels and abnormal retinal vascular growth. The unchecked vascular growth was driven by the protein vascular endothelial growth factor (Vegfa). When the light response pathway is properly engaged, it modulates Vegfa to help prevent promiscuous vascular growth, according to researchers.

The melanopsin protein is present in both mice and humans during pregnancy. Lang said the research team is continuing to study how the light-response pathway might influence the susceptibility of pre-term infants to retinopathy of prematurity and also be related to other diseases of the eye.

First author on the study was Sujata Rao, PhD, a member of Lang’s laboratory team. Funding support for the research came in part from the National Institutes of Health (NIH AR-47363) and the Abrahamson Pediatric Eye Institute at Cincinnati Children’s.

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The above story is reprinted from materials provided by Cincinnati Children’s Hospital Medical Center.

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Journal Reference:

1. Sujata Rao, Christina Chun, Jieqing Fan, J. Matthew Kofron, Michael B. Yang, Rashmi S. Hegde, Napoleone Ferrara, David R. Copenhagen, Richard A. Lang. A direct and melanopsin-dependent fetal light response regulates mouse eye development. Nature, 2013; DOI: 10.1038/nature11823

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Jan. 11, 2013 — A new Investigative Ophthalmology & Visual Science (IOVS) article reveals that increasingly aggressive therapies that block VEGF could cause damage in treating eye diseases. Scientists discovered inhibiting anti-VEGF might have a harmful effect on the tissue responsible for producing the fluid that bathes the eye, medically termed the ciliary body.

“Very little is known about the factors that regulate the integrity and function of this tissue the ciliary body in the adult,” said author Patricia A. D’Amore, PhD, of Schepens Eye Research Institute/Massachusetts Eye and Ear. “Our finding indicates that VEGF-A is at least one of the molecules that play a role in keeping the ciliary body healthy and functioning properly.”

In the study, Expression and role of VEGF-A in the Ciliary Body, investigators simulated the VEGF-A activity in adult mice and found that blocking the protein decreased the intraocular pressure, an unexpected side effect that impaired the ciliary body.

Several anti-VEGF-A therapies are currently being widely and successfully used for the treatment of eye diseases like wet macular degeneration, diabetic macular edema and retinopathy of prematurity. D’Amore agrees that there is no evidence to indicate that the manner in which these drugs are being administered interferes with the ciliary body. “However, there is a move toward developing methods to continuously deliver anti-VEGF to the eye and to have drugs that are more potent inhibitors of VEGF,” she said. “I would be concerned that more aggressive VEGF inhibition in the eye would have deleterious effects on the ciliary body.”

The research team’s investigation of anti-VEGF-A on the ciliary body was the result of prior studies that found blocking VEGF can lead to the degeneration of capillary beds, particularly capillaries that have specializations called fenestrations like the ones found in the ciliary body. These include whole body VEGF blockade in anti-cancer therapies that damage the capillaries of the kidney and the effect anti-VEGF has had on the thyroid function in people treated locally for brain tumors.

The results of the new IOVS study suggest further research, including clinical trials, should be considered. “I am hoping that revealing the possible negative side effects of VEGF inhibition in the eye will motivate research into new ways to block edema and blood vessel growth in the eye that does not require continuous inhibition of intraocular VEGF,” said D’Amore.

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The above story is reprinted from materials provided by Association for Research in Vision and Ophthalmology (ARVO), via Newswise.

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Journal Reference:

1. K. M. Ford, M. Saint-Geniez, T. E. Walshe, P. A. D’Amore. Expression and Role of VEGF-A in the Ciliary Body. Investigative Ophthalmology & Visual Science, 2012; 53 (12): 7520 DOI: 10.1167/iovs.12-10098

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Jan. 2, 2013 — A new study finds that certain changes in blood vessels in the eye’s retina can be an early warning that a person is at increased risk for glaucoma, an eye disease that slowly robs people of their peripheral vision. Using diagnostic photos and other data from the Australian Blue Mountains Eye Study, the researchers showed that patients who had abnormally narrow retinal arteries when the study began were also those who were most likely to have glaucoma at its 10-year end point. If confirmed by future research, this finding could give ophthalmologists a new way to identify and treat those who are most vulnerable to vision loss from glaucoma.

The study was recently published online by Ophthalmology, the journal of the American Academy of Ophthalmology.

Open-angle glaucoma (OAG), the most common form of the disease, affects nearly three million people in the U.S and 60 million worldwide. Vision loss occurs when glaucoma damages the optic nerve, the part of the eye that transmits images from the retina to the brain. Unfortunately, because glaucoma does not have symptoms, many people don’t know they have the disease until a good portion of their sight has been lost. Early detection is critical to treating glaucoma in time to preserve vision.

The findings of the new study, led by Paul Mitchell, M.D., PhD, of the Centre for Vision Research, University of Sydney, supports the concept that abnormal narrowing of retinal blood vessels is an important factor in the earliest stages of OAG. Tracking nearly 2,500 participants, the study found that the OAG risk at the 10-year mark was about four times higher in patients whose retinal arteries had been narrowest when the study began, compared with those who had had the widest arteries.

None of the participants had a diagnosis of OAG at the study’s outset. Compared with the study group as a whole, the patients who were diagnosed with OAG by the 10-year mark were older, had had higher blood pressure or higher intraocular pressure at the study’s baseline, and were more likely to be female. Elevated intraocular pressure, or pressure within the eye, is often found in patients with OAG. Study results were adjusted for age, family history of glaucoma, smoking, diabetes, hypertension, and other relevant factors.

“Our results suggest that a computer-based imaging tool designed to detect narrowing of the retinal artery caliber, or diameter, could effectively identify those who are most at risk for open-angle glaucoma,” said Dr. Mitchell. “Such a tool would also need to account for blood pressure and other factors that can contribute to blood vessel changes. Early detection would allow ophthalmologists to treat patients before optic nerve damage occurs and would give us the best chance of protecting their vision.”

A symptomless eye disease like glaucoma highlights the importance of regular eye exams. The American Academy of Ophthalmology recommends that everyone have a complete eye exam by an ophthalmologist at age 40 and stick to the follow-up exam schedule advised by their doctor.

This January during Glaucoma Awareness Month, the Academy encourages people to learn more about the disease known as “the sneak thief of sight.” People who have a family history of glaucoma, or who are African-American or Hispanic, may be at higher risk.

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The above story is reprinted from materials provided by American Academy of Ophthalmology, via Newswise.

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Journal Reference:

1. Ryo Kawasaki,
   Jie Jin Wang,

   Elena Rochtchina,
   Anne J. Lee,
   Tien Yin Wong,
   Paul Mitchell. Retinal Vessel Caliber Is Associated with the 10-year Incidence of Glaucoma: The Blue Mountains Eye Study. Ophthalmology, 2013 DOI: 10.1016/j.ophtha.2012.07.007

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Dec. 21, 2012 — Branch retinal vein occlusion — blockage of the blood vessels that channel blood from the retina — is a common eye disease. A type of blood clot in the eye, the disease causes reduced vision, and people with the disease also typically have an increased risk of hypertension, diabetes and other serious conditions. A young scientist from the University of Copenhagen has made a significant contribution to finding the cause of the disease.

A team of researchers at the University of Copenhagen, Glostrup Hospital and several other ophthalmology departments at Danish hospitals have now shown that it is highly probable that thickening of the arterial walls is behind the common eye disease known as branch retinal vein occlusion — a type of blood clot in the eye that blocks the vessels that transport blood from the retina. The disease leads to reduced vision and affects more than 14 million people worldwide.

“Our new results indicate that branch retinal vein occlusion is caused by thickening of the arterial wall. This makes it crucial for doctors to treat patients diagnosed with the disease with medicine to lower blood pressure in order to prevent blood clots from forming in the heart and brain. Branch retinal vein occlusion is often a sign of increased risk of blood clots in other parts of the body,” explains Mette Bertelsen, PhD student at the University of Copenhagen.

Targeted treatment

Mette Bertelsen, head of the research project, and her colleagues photographically verified the diagnosis of branch retinal vein occlusion in 1168 people. They identified the patients’ other diseases with the help of Danish national registries and compared the data to that of 116.800 healthy people.

By looking at the illness and mortality statistics of Danes diagnosed with a blood clot in the retina’s main blood vessels, both before and after the occurrence of the retinal blood clot, Mette Bertelsen and her colleges has now shown that while these patients show a higher frequency of arterial disease in the heart and brain, they do not display a higher frequency of venous disease. This new knowledge, which has been published in the British Medical Journal, means that disease prevention and treatment of these patients should be targeted at hypertension, diabetes and atherosclerosis, while doctors can save patients from unnecessary treatment with anticoagulants.

Thickened arteries the villains

Doctors have long debated the three most likely theories about what causes branch retinal vein occlusion. Discussion centres on whether the disease is due to a) conditions in the veins that cause blood clots, b) a change in the composition of the blood, or c) blockage of the vein due to compression from an adjacent artery that has thickened and thus compresses the vein and hinders blood flow.

“To understand what is actually happening, it can be helpful to picture a garden hose that has been squeezed by a larger hose, cutting off the water supply. That is essentially what happens when a vein is compressed by a thickened artery. Clearly, the consequences can be serious,” explains Mette Bertelsen. She adds that no one knows exactly how many Danes suffer from branch retinal vein occlusion, but that more than 14 million people have the disease worldwide.

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The above story is reprinted from materials provided by University of Copenhagen.

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Journal Reference:

1. M. Bertelsen, A. Linneberg, T. Rosenberg, N. Christoffersen, H. Vorum, E. Gade, M. Larsen. Comorbidity in patients with branch retinal vein occlusion: case-control study. BMJ, 2012; 345 (nov30 1): e7885 DOI: 10.1136/bmj.e7885

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Dec. 11, 2012 — A new study published in Investigative Ophthalmology & Visual Science found that between 40 to 50 percent of older adults with visually impairing eye disease limit their activities due to a fear of falling. Vision scientists warn that this protective strategy puts seniors at risk for social isolation and disability.

In the paper, “Activity Limitation Due to a Fear of Falling in Older Adults with Eye Disease,” researchers report on their examination of patients with age-related macular degeneration (AMD), glaucoma and Fuchs corneal dystrophy, as compared to a control group of older adults with good vision. Of the three groups with visual limitations, the patients with Fuchs corneal dystrophy were the mostly like to report activity limitation due to fear of falling, followed by those with glaucoma and the AMD group.

“I expected all of the groups to limit their activities due to a fear of falling but I was a bit surprised that the group with Fuchs corneal dystrophy was the most likely to limit their activities,” says Ellen E. Freeman, PhD, Department of Ophthalmology at the University of Montreal, Québec, Canada. “I was also surprised at how frequently people with eye disease reported limiting their activities due to fear of falling. Clearly, this is something that is affecting many people with eye disease.”

The research team conducted a cross-sectional study of 345 patients (93 with AMD, 57 with Fuchs, 98 with glaucoma and 97 controls) from the ophthalmology clinics of Maisonneuve-Rosemont Hospital in Montreal. Questionnaires and vision tests were given to each patient. Only 16 percent of controls with normal vision reported activity limitation due to a fear of falling compared with the 40 to 50 percent of patients with eye disease.

Results also showed that people who reported activity limitation due to a fear of falling were older, were more likely to be females, had worse vision, were more likely to be depressed and had greater comorbidity.

Freeman points out that their findings are not only relevant to older patients with eye disease, but to their families, physicians and to those providing low vision rehabilitation services. “It is important to know more about which activities are being limited due to fear of falling. We can then develop and test interventions to help people feel more confident about their ability to safely do those activities,” she says. ” If we could develop a brief, effective intervention focused on select activities, I would like to see it offered in the clinical setting. Then, we could encourage people to see a low vision rehabilitation specialist if they want more training.”

The research team concludes that older adults with eye disease should stay as mobile as safely possible to help prevent morbidity associated with a sedentary lifestyle, mobility disability and mortality.

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Journal Reference:

1. M. Y. Wang, J. Rousseau, H. Boisjoly, H. Schmaltz, M.-J. Kergoat, S. Moghadaszadeh, F. Djafari, E. E. Freeman. Activity Limitation due to a Fear of Falling in Older Adults with Eye Disease. Investigative Ophthalmology & Visual Science, 2012; 53 (13): 7967 DOI: 10.1167/iovs.12-10701

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Dec. 11, 2012 — A new study published in Investigative Ophthalmology & Visual Science found that between 40 to 50 percent of older adults with visually impairing eye disease limit their activities due to a fear of falling. Vision scientists warn that this protective strategy puts seniors at risk for social isolation and disability.

In the paper, “Activity Limitation Due to a Fear of Falling in Older Adults with Eye Disease,” researchers report on their examination of patients with age-related macular degeneration (AMD), glaucoma and Fuchs corneal dystrophy, as compared to a control group of older adults with good vision. Of the three groups with visual limitations, the patients with Fuchs corneal dystrophy were the mostly like to report activity limitation due to fear of falling, followed by those with glaucoma and the AMD group.

“I expected all of the groups to limit their activities due to a fear of falling but I was a bit surprised that the group with Fuchs corneal dystrophy was the most likely to limit their activities,” says Ellen E. Freeman, PhD, Department of Ophthalmology at the University of Montreal, Québec, Canada. “I was also surprised at how frequently people with eye disease reported limiting their activities due to fear of falling. Clearly, this is something that is affecting many people with eye disease.”

The research team conducted a cross-sectional study of 345 patients (93 with AMD, 57 with Fuchs, 98 with glaucoma and 97 controls) from the ophthalmology clinics of Maisonneuve-Rosemont Hospital in Montreal. Questionnaires and vision tests were given to each patient. Only 16 percent of controls with normal vision reported activity limitation due to a fear of falling compared with the 40 to 50 percent of patients with eye disease.

Results also showed that people who reported activity limitation due to a fear of falling were older, were more likely to be females, had worse vision, were more likely to be depressed and had greater comorbidity.

Freeman points out that their findings are not only relevant to older patients with eye disease, but to their families, physicians and to those providing low vision rehabilitation services. “It is important to know more about which activities are being limited due to fear of falling. We can then develop and test interventions to help people feel more confident about their ability to safely do those activities,” she says. ” If we could develop a brief, effective intervention focused on select activities, I would like to see it offered in the clinical setting. Then, we could encourage people to see a low vision rehabilitation specialist if they want more training.”

The research team concludes that older adults with eye disease should stay as mobile as safely possible to help prevent morbidity associated with a sedentary lifestyle, mobility disability and mortality.

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The above story is reprinted from materials provided by Association for Research in Vision and Ophthalmology, via Newswise.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Journal Reference:

1. M. Y. Wang, J. Rousseau, H. Boisjoly, H. Schmaltz, M.-J. Kergoat, S. Moghadaszadeh, F. Djafari, E. E. Freeman. Activity Limitation due to a Fear of Falling in Older Adults with Eye Disease. Investigative Ophthalmology & Visual Science, 2012; 53 (13): 7967 DOI: 10.1167/iovs.12-10701

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

ScienceDaily (Nov. 27, 2012) — Herbs widely used throughout history in Asian and early European cultures have received renewed attention by Western medicine in recent years. Scientists are now isolating the active compounds in many medicinal herbs and documenting their antioxidant and anti-inflammatory activities. In a study published in the journal Investigative Ophthalmology & Visual Science, Stuart A. Lipton, M.D., Ph.D. and colleagues at Sanford-Burnham Medical Research Institute (Sanford-Burnham) report that carnosic acid, a component of the herb rosemary, promotes eye health.

Lipton’s team found that carnosic acid protects retinas from degeneration and toxicity in cell culture and in rodent models of light-induced retinal damage. Their findings suggest that carnosic acid may have clinical applications for diseases affecting the outer retina, including age-related macular degeneration, the most common eye disease in the U.S.

Age-related macular degeneration

Age-related macular degeneration likely has many underlying causes. Yet previous studies suggest that the disease might be slowed or improved by chemicals that fight free radicals — reactive compounds related to oxygen and nitrogen that damage membranes and other cell processes.

Lipton’s team first discovered a few years ago that carnosic acid fights off free radical damage in the brain. In their latest study, Lipton and colleagues, including Tayebeh Rezaie, Ph.D. and Takumi Satoh, Ph.D., initially investigated carnosic acid’s protective mechanism in laboratory cultures of retinal cells.

The researchers exposed the cells growing in the dish to hydrogen peroxide in order to induce oxidative stress, a factor thought to contribute to disease progression in eye conditions such as macular degeneration and retinitis pigmentosa. They found that cells treated with carnosic acid triggered antioxidant enzyme production in the cells, which in turn lowered levels of reactive oxygen and nitrogen species (cell-damaging free radicals and peroxides).

Rosemary’s therapeutic potential

Lipton, Rezaie, Satoh and colleagues next tested carnosic acid in an animal model of light-induced damage to photoreceptors — the part of the eye that converts light to electrical signals, enabling visual perception. As compared to the untreated group, rodents pre-treated with carnosic acid retained a thicker outer nuclear layer in the eye, indicating that their photoreceptors were protected. The carnosic acid-treated rodents also exhibited better electroretinogram activity, a measure of healthy photoreceptor function.

What’s next for carnosic acid? “We’re now developing improved derivatives of carnosic acid and related compounds to protect the retina and other brain areas from a number of degenerative conditions, including age-related macular degeneration and various forms of dementia,” said Lipton, director of Sanford-Burnham’s Del E. Webb Neuroscience, Aging, and Stem Cell Research Center and an active clinical neurologist.

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The above story is reprinted from materials provided by Sanford-Burnham Medical Research Institute, via EurekAlert!, a service of AAAS.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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Journal Reference:

1. T. Rezaie, S. R. McKercher, K. Kosaka, M. Seki, L. Wheeler, V. Viswanath, T. Chun, R. Joshi, M. Valencia, S. Sasaki, T. Tozawa, T. Satoh, S. A. Lipton. Protective effect of carnosic acid, a pro-electrophilic compound, in models of oxidative stress and light-induced retinal degeneration. Investigative Ophthalmology & Visual Science, 2012; DOI: 10.1167/iovs.12-10793

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.