Early Diagnosis and Treatment Can Lessen Effects of Glaucoma, the “Sneak Thief of Sight”

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Posted on 28th January 2013 by Pacific ClearVision Institute in General |Retina

American Optometric Association emphasizes importance of comprehensive eye exams during National Glaucoma Awareness Month

Studies show that over the next 10 years the number of Americans diagnosed with glaucoma will increase by more than one million. The American Optometric Association (AOA) urges people of all ages to take control of their eye health through early detection to help minimize the risk of developing glaucoma, a disease that damages the optic nerve and often results in loss of sight.

Glaucoma is the second leading cause of blindness in the U.S.; however, awareness surrounding the disease is relatively low. According to data from the AOA’s latest American Eye-Q® consumer survey:

- 90 percent of respondents think glaucoma is preventable-only 10 percent know it’s not, but that it’s treatable
- 86 percent don’t know what part of vision glaucoma affects-deterioration to peripheral vision making it hard to see
- 72 percent think glaucoma has early warning signs…it does not. Only an exam that dilates the eyes can show what’s going on

Regular eye exams are the first line of defense for early detection of glaucoma, according to the AOA. The disease often strikes without pain or other symptoms, so it is crucial for patients to receive a dilated eye exam where their eye doctor can thoroughly examine the pressure and nerves inside the eyes for potential signs of the disease.

Americans are not aware of the factors that put them most at risk for developing glaucoma: 86 percent of American Eye-Q® respondents are unaware that a person’s race places them at a higher risk of developing glaucoma. According to the Glaucoma Research Foundation, glaucoma is six to eight times more common in African Americans than Caucasians. Other risk factors include those who have a family history of glaucoma, hypothyroidism, are over age 60, or individuals who have had severe eye trauma.

Treatment for glaucoma includes prescription eye drops and medicines to lower pressure in the eyes. In some cases, laser treatment or surgery may be effective in reducing pressure.

Accelerated Corneal Crosslinking Procedure Receives CE Approval; Designed to Strengthen Eye Surface After LASIK

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Posted on 28th January 2013 by Pacific ClearVision Institute in General |LASIK

A procedure called Lasik Xtra, which is designed to strengthen the cornea after LASIK, has received CE approval for marketing in the European Union. It was just approved in Canada as well.

Marketed by Avedro, Inc., Lasik Xtra is a corneal crosslinking procedure that applies the company’s VibeX riboflavin ophthalmic solution to the eye’s surface (cornea), and then uses Avedro’s KXL System to irradiate the cornea with UV-A rays. Lasik Xtra is an accelerated form of crosslinking — Avedro says it takes two minutes — which makes it more convenient to combine with LASIK.

Avedro said that in April it will report on studies that show the procedure has helped people who received hyperopic LASIK, which tends to regress more than myopic LASIK, to maintain the vision correction they had received from LASIK.

Although corneal crosslinking has not received FDA approval yet, Avedro’s VibeX solution has received orphan drug approvals from the agency. Orphan drug status is usually conferred on treatments for rare medical conditions (in this case, keratoconus, which is a gradual thinning of the cornea).

Light Exposure During Pregnancy Key to Normal Eye Development

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Posted on 28th January 2013 by Pacific ClearVision Institute in General |Retina

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.

Light Shed On Complexity of Gene Therapy for Congenital Blindness

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Posted on 28th January 2013 by Pacific ClearVision Institute in General |Retina

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.

Altering Eye Cells May One Day Restore Vision

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Posted on 28th January 2013 by Pacific ClearVision Institute in General |Retina

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.

January is National Glaucoma Awareness Month

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Posted on 10th January 2013 by Pacific ClearVision Institute in General |Retina

Sight Unseen: Glaucoma Takes Sight without Warning—How to Protect Yourself?

What are you going to do differently this year? Take better care of yourself? Will you exercise more, eat healthier, or make an effort to see the doctor as often as you should?

Finding time in your busy schedule to implement those well-intentioned resolutions often proves challenging. But don’t underestimate the importance of those doctor visits – and more specifically, visits to your eye doctor.

A quick trip to your optometrist may not only be sight-saving but potentially life-saving. Optometrists can evaluate the health of your eyes and clarity of vision and they can also detect chronic and systemic diseases such as glaucoma, diabetes and even hypertension.

You’ve probably heard of glaucoma, but many people don’t know how it can affect – and how quickly it can take – your eyesight. Glaucoma affects more than three million Americans, but over half of them don’t even know that they have it, according to Prevent Blindness America.

Glaucoma begins by attacking peripheral vision, typically causing objects to appear less clearly. At first, it is possible to compensate by squinting or turning the head to focus better. But be careful. These changes may seem minor, but glaucoma can accelerate quickly; causing eyesight to rapidly and irreversibly deteriorate.

Like many diseases, some factors can increase the risk of developing glaucoma, such as age, race or genetics. Glaucoma usually affects one in 200 people by age 50, but as many as one in 10 people by age 80. The risk of developing glaucoma is much higher among African Americans: four to five times higher. In fact, glaucoma is the leading cause of blindness in African Americans. Not only do African Americans usually develop glaucoma 10 years earlier than Caucasians, they are also six to 15 times more likely to be blinded by the disease.

Glaucoma cannot be prevented, but if diagnosed and treated early, it can be controlled. This reinforces what the National Optometric Association and the AOA already recommend: adults need regular, comprehensive eye exams. Fortunately, Medicare covers annual glaucoma screenings for people considered at heightened risk of developing glaucoma, such as individuals with diabetes, those with a family history of glaucoma, African Americans age 50 and older and Hispanic Americans age 65 and older.

So start off the new year right: set up an appointment with your eye doctor – and maybe hit the gym and grab a salad on your way home.

Medicare patients at high risk for glaucoma can receive dilated eye examinations as a benefit of Medicare coverage. Currently eligible beneficiaries are individuals with diabetes mellitus, individuals with a family history of glaucoma, Hispanic-Americans age 65 and over, and African-Americans age 50 and over. The AOA provides a Glaucoma/Diabetes Hotline program which matches patients with participating optometrists in their area. To find an optometrist in your area, please call 800-262-3947.

Courtesy Of: American Optometric Association