Glaucoma as Neurologic Disorder Rather Than Eye Disease?

ScienceDaily (Mar. 7, 2012) - A new paradigm to explain Glaucoma is rapidly emerging, and it is generating brain-based treatment advances that may ultimately vanquish the disease known as the "sneak thief of sight." A review now available in Ophthalmology, the journal of the American Academy of Ophthalmology, reports that some top researchers no longer think of Glaucoma solely as an eye disease. Instead, they view it as a neurologic disorder that causes nerve cells in the brain to degenerate and die, similar to what occurs in Parkinson disease and in Alzheimer's. The review, led by Jeffrey L Goldberg, M.D., Ph.D., assistant professor of ophthalmology at the Bascom Palmer Eye Institute and Interdisciplinary Stem Cell Institute, describes treatment advances that are either being tested in patients or are scheduled to begin clinical trials soon.

Glaucoma is the most common cause of irreversible blindness worldwide. For many years, the prevailing theory was that vision damage in Glaucoma patients was caused by abnormally high pressure inside the eye, known as intraocular pressure (IOP). As a result, lowering IOP was the only goal of those who developed surgical techniques and medications to treat Glaucoma. Creating tests and instruments to measure and track IOP was crucial to that effort. Today, a patient's IOP is no longer the only measurement an ophthalmologist uses to diagnose Glaucoma, although it is still a key part of deciding how to care for the patient. IOP-lowering medications and surgical techniques continue to be effective ways to protect Glaucoma patients' eyes and vision. Tracking changes in IOP over time informs the doctor whether the treatment plan is working.

But even when surgery or medication successfully lowers IOP, vision loss continues in some Glaucoma patients. Also, some patients find it difficult to use eye drop medications as prescribed by their physicians. These significant shortcomings spurred researchers to look beyond IOP as a cause of Glaucoma and focus of treatment.

The new research paradigm focuses on the damage that occurs in a type of nerve cell called retinal ganglion cells (RGCs), which are vital to the ability to see. These cells connect the eye to the brain through the optic nerve.

RGC-targeted Glaucoma treatments now in clinical trials include: medications injected into the eye that deliver survival and growth factors to RGCs; medications known to be useful for stroke and Alzheimer's, such as cytidine-5-diphosphocholine; and electrical stimulation of RGCs, delivered via tiny electrodes implanted in contact lenses or other external devices. Human trials of stem cell therapies are in the planning stages.

"As researchers turn their attention to the mechanisms that cause retinal ganglion cells to degenerate and die, they are discovering ways to protect, enhance and even regenerate these vital cells," said Dr. Goldberg. "Understanding how to prevent damage and improve healthy function in these neurons may ultimately lead to sight-saving treatments for Glaucoma and other degenerative eye diseases."

If this neurologically-based research succeeds, future Glaucoma treatments may not only prevent Glaucoma from stealing patients' eyesight, but may actually restore vision. Scientists also hope that their in-depth exploration of RGCs will help them determine what factors, such as genetics, make some people more vulnerable to Glaucoma.

http://www.sciencedaily.com/releases/2012/03/120307094659.htm

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Vitamin B-Based Treatment for Corneal Disease May Offer Some Patients a Permanent Solution

ScienceDaily (Oct. 24, 2011) - Patients in the United States who have the Cornea-damaging disease keratoconus may soon be able to benefit from a new treatment that is already proving effective in Europe and other parts of the world. The treatment, called collagen crosslinking, improved vision in almost 70 percent of patients treated for keratoconus in a recent three-year clinical trial in Milan, Italy. The treatment is in clinical trials in the United States and is likely to receive FDA approval in 2012.

The results of the Milan study are being presented Oct. 24, 2011 at the 115th Annual Meeting of the American Academy of Ophthalmology in Orlando, Florida.

In a session titled Long-term Results of Corneal Crosslinking for Keratoconus, Paolo Vinciguerra, MD will describe the treatment and three-year follow up of more than 250 keratoconus patients who received collagen crosslinking at his clinic. Sixty-eight percent of the 500 eyes treated gained significant visual acuity, with their results remaining stable at the end of the follow-up period. Patients over age 18 were most likely to improve.

In the collagen crosslinking procedure, riboflavin (vitamin B) is applied to the Cornea, which is then exposed to a specific form of ultraviolet light. Collagen fibers regenerate with new bonds forming between them, increasing Corneal stiffness and strength. The treatment also combats the causes of keratoconus, reducing the chance that it will recur. The rest of the eye receives only minimal UV exposure during treatment. Dr. Vinciguerra's new study confirms that adverse effects are rare. Previous research by his team indicated no loss of Corneal endothelial cell, a measurement used to assess the safety of Corneal treatments, in patients who received collagen crosslinking.

"For many people with keratoconus, collagen crosslinking can provide a better and more permanent solution to their vision problems," said Dr. Vinciguerra. "Given that no current treatment in use in the U.S. offers permanent correction, this effective option represents a significant advance for Corneal medicine."

One in 2,000 people in the United States and worldwide are diagnosed with keratoconus, a disease that damages the collagen fibers that form the structure of the Cornea, which is the outer surface of the eye. The Cornea's crucial task is to focus, or "refract," incoming light toward the eye's lens. To perform properly, the Cornea needs to be rounded, like the surface of a ball. As keratoconus worsens and the Cornea becomes thinner, it may bulge outward in a cone shape, causing nearsightedness and/or astigmatism, making clear vision impossible. As the number of fibers and links between them decline, the Cornea loses up to 50 percent of its normal stiffness.

Standard treatments in the U.S., such as specialized eyeglasses, contact lenses, or implanted lenses, cannot permanently correct keratoconus, and none of these treatments address the underlying causes. Severe keratoconus often requires Corneal transplant.

The 115th Annual Meeting of the American Academy of Ophthalmology is in session October 23 through 25 at the Orange County Convention Center in Orlando, Fla. It is the world's largest, most comprehensive ophthalmic education conference. Approximately 25,000 attendees and more than 500 companies gather each year to showcase the latest in ophthalmic technology, products and services. To learn more about the place Where All of Ophthalmology Meets visit www.aao.org/annual_meeting.

http://www.sciencedaily.com/releases/2011/10/111024084641.htm

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Detecting Glaucoma Before It Blinds

Early detection and diagnosis of open angle Glaucoma important so that treatment can be used in the early stages of the disease developing to prevent or avoid further vision loss. Writing in a forthcoming issue of the International Journal of Medical Engineering and Informatics, researchers in the US have analyzed and ranked the various risk factors for open angle Glaucoma so that patients can be screened at an earlier stage if they are more likely to develop the condition.

Glaucoma is one of the main leading causes of blindness; it is a progressive and irreversible disease. Of the various forms of Glaucoma, open angle Glaucoma (OAG) is the most common and can cause the most damage. Unfortunately, unless a patient is undergoing regular screening from about the age of 40 years because of a family history, it is otherwise difficult to detect until substantial and irreversible vision loss has occurred. Glaucoma is the third leading cause of blindness worldwide and the second leading cause of blindness in the USA.

Now, Duo Zhou and colleagues at the University of Medicine and Dentistry of New Jersey, Newark, have used statistical collinearity analysis to evaluate risk factors for OAG, and logistic regression models to identify a minimum set of such risk factors for prognosis and diagnosis of the disease. Their study was based on more than 400 patients with subtle or severe vision problems who attended hospital. It reveals the relative risk of being a smoker, age, visual "field test" results, presence of a localized notch or thinning of the neuroretinal rim identified during standard eye examination, cup to disk ratio (a measure of restriction of the optic nerve at the back of the eye) and other factors.

The data are complex and separating out predictors from diagnostic factors was difficult, the team admits. However, they suggest that family history, medical history, current medications, geographic location, visual field test and ocular examination must all be considered in diagnosis and prognosis for OAG. They have excluded certain factors from the OAG prognosis: gender, race, family history of Glaucoma, diabetes mellitus, hypercholesterolemia, thyroid disease, migraine, Reynaud's disease and myopia as these have no direct effect on OAG development.

As revealed in the analyses, the odds of developing OAG will be increased by 91% with an increase in the Cup-to-Disc ratio of 0.1. Risk increases by 3% annually by age but decreases by 31% for every dB increase of mean deviation of Humphrey visual field. The odds of developing OAG will be 4.36 higher for patients with abnormal Humphrey visual filed overall test, 7.19 higher in patients with localized notch or thinning of the neuroretinal rim. Interestingly, patients with a smoking history seem to be less likely to develop OAG as compared to those with smoking history; although there are many smokers with OAG. Oddly, because of the location of the study, the team can also say that patients living in Atlantic/Quebec will be 73% less likely to develop OAG compared to their fellow Canadians in Ontario.

http://www.sciencedaily.com/releases/2011/10/111006094823.htm

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Do your eyes hold the secret of life?

In the future, patients in need of perfectly matched neural stem cells may not need to look any further than their own eye.

Researchers reporting in the January issue of Cell Stem Cell, a Cell Press publication, have identified adult stem cells of the central nervous system in a single layer of cells at the back of the eye.

That cell layer, known as the retinal pigment epithelium (RPE), underlies and supports photoreceptors in the light-sensitive retina. Without it, photoreceptors and vision are lost. The new study shows that the RPE also harbors self-renewing stem cells that can wake up to produce actively growing cultures when placed under the right conditions. They can also be coaxed into forming other cell types.

"You can get these cells from a 99-year-old," said Sally Temple of the Neural Stem Cell Institute in Rensselaer, New York. "These cells are laid down in the embryo and can remain dormant for 100 years. Yet you can pull them out and put them in culture and they begin dividing. It is kind of mind boggling."

Temple's group got the RPE-derived stem cells they describe from the eye of donors in the hours immediately after their deaths. But the cells can also be isolated from the fluid that surrounds the retina at the back of the eye, which means they are accessible in living people as well.

"You can literally go in and poke a needle in the eye and get these cells from the subretinal space," she says. "It sounds awful, but retinal surgeons do it every day." By comparison, access to most other neural stem cell populations would require major surgery.

Temple said they were curious about the proliferative potential of the RPE given that the tissue is known to be capable of regenerating entire retinas in salamanders. But that plasticity in adulthood had seemed to be lost in mice and chicks. Still, "given the evolutionary evidence, we thought it was worth revisiting," she said.

They placed RPE tissue taken from 22-year-old to 99-year-old cadavers into many culture conditions to see what they could make the cells do. They found one set of conditions that got the cells dividing. Not all of the RPE cells have this regenerative potential, but perhaps 10 percent of them do.

Further work showed that the cells are multipotent, which means that they can form different cell types, though the researchers admit there is more to do to fully explore the cells' differentiation capacity.

There are other implications as well. For example, these cells may explain diseases in which other tissue types show up in the eye. Their presence also suggests that there might be some way to stimulate controlled repair of the eye in the millions of people who suffer from age-related macular degeneration.

"I think it might be possible," Temple said.

http://www.sciencedaily.com/releases/2012/01/120105131637.htm

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Gene therapy to treat diseases that cause blindness.

cornea Gene Discovery Reveals Why Humans See Clearly

A transparent cornea is essential for vision, which is why the eye has evolved to nourish the cornea without blood vessels. But for millions of people around the world, diseases of the eye or trauma spur the growth of blood vessels and can cause blindness.

A new Northwestern Medicine study has identified a gene that plays a major role in maintaining clarity of the cornea in humans and mice -- and could possibly be used as gene therapy to treat diseases that cause blindness. The paper is published in the Proceedings of the National Academy of Sciences.

"We believe we've discovered the master regulator gene that prevents the formation of blood vessels in the eye and protects the clarity of the cornea," said lead author Tsutomu Kume, associate professor of medicine at Northwestern University Feinberg School of Medicine and a researcher at Feinberg Cardiovascular Research Institute.

The existence of the gene, FoxC1, was previously known, but its role in maintaining a clear cornea is a new finding. Working with a special breed of mice that are missing this gene, Kume and colleagues found abnormal vascular formations, or blood vessels, streaking their corneas and blocking light.

When Kume discovered the corneal blood vessels in the mutant mice, he called a collaborator at the University of Alberta in Canada, Ordan Lehmann, MD, professor of ophthalmology and medical genetics.

Lehmann found that his patients who have a single copy of this mutated FoxC1 gene -- and who have congenital glaucoma -- also have abnormal blood vessel growth in their eyes.

"The exciting thing is by showing the loss of FoxC1 causes vascularization of the cornea, it means increasing levels of the gene might help prevent the abnormal growth of blood vessels, potentially in multiple eye disorders that cause blindness," said Lehmann, a coauthor on the paper. "That's the hope." One possible use might be in corneal transplants, he said, where the growth of new blood vessels onto the transplanted cornea is a major problem.

Kume next plans to test the gene therapy in mice to see if injecting FoxC1 inhibits the formation of blood vessels in the cornea.

The research is funded by National Institutes of Health and Canadian Institutes of Health Research.

ScienceDaily (Dec. 12, 2011)

http://www.sciencedaily.com/releases/2011/12/111212153121.htm

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The above story is reprinted from materials provided byNorthwestern University. The original article was written by Marla Paul.

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How to make checking in at your doctor's office EASY!

Knowing your insurance coverage and how your benefits work will make checking in with the front desk easier on you and your wallet. Look into your vision and medical benefits before you arrive for your appointment by visiting your insurance WEBSITE online or call the member services number on the back of your cards FOR A DESCRIPTION OF YOUR BENEFITS. If you are unsure of your coverage you can always call your Human Resource department at your place of employment.

Bring both your medical and vision benefit cards or information with you to the appointment. When you provide us with the correct information we can verify coverage and sometimes, even the exact dollar amount towards glasses or contact lenses.

Know your copay and be prepared to pay it at the time of your visit. Knowing your coverage helps us help you maximize the coverage you can receive!