The conclusions are not as clear-cut in the area of antioxidant and zinc supplements. Although animal studies have demonstrated a correlation between a deficiency in vitamin A or E and degeneration of the retina, it's not known if these deficiencies lead to AMD, or make it progress faster. The data provided by various human studies are conflicting, but there is some evidence that high blood levels of vitamins C and E and the carotenoids are associated with a reduced risk of AMD. The soon-to-be-released Age-related Eye Disease Study, sponsored by the National Eye Institute, will provide more data in this area. In the meantime, experts agree that taking a multivitamin each day and eating a diet that includes dark, green leafy vegetables, such as spinach, kale, turnip and collard greens, can't hurt, and may help. Zarbin warns against self-administered regimens of vitamins and zinc, when no deficiency has been shown, since "megadoses" of vitamins and minerals can be dangerous.

Another major question to be answered is what role genetics plays in the development of age-related macular degeneration. Data has shown that when one twin has AMD, the likelihood of the other developing it is high; and that about 15 percent of those with AMD have a close relative with the disease. In 1997, researchers reported that a variant of a gene known to cause a rare type of macular degeneration affecting children and young adults - called Stargardt disease - may be implicated in about 15 percent of AMD cases. Investigators think that multiple genes may be involved when there is an inherited predisposition.

Those who already have the disease, or are at high risk for developing it, are most interested in effective therapies. At this moment, there is no proven treatment for the dry form. Zarbin explains that laser therapy to reduce the number of drusen is being tested, although their elimination does not necessarily lead to improved vision. "It is hoped that eliminating drusen will reduce the chance for CNV development," he says. The good news is that the disease tends to progress very slowly, and there are many high-tech optical aids that may be of help to those with impaired vision.

The only proven effective therapy for the wet form of AMD is laser photocoagulation, which seals the leaking blood vessels . Unfortunately, only 10 to 20 percent of affected patients are candidates for the treatment, which destroys some healthy retinal tissue as well, and is frequently just a temporary stopgap. "In about half of those treated with lasers, abnormal blood vessels will grow again within 18 months. Still, laser treatment is generally better than no treatment in properly selected patients," says Zarbin.

Clinical trials for a new "photodynamic" therapy have just been completed. Zarbin says it may prove to be the first major effective new treatment for AMD in a decade. It uses a light-activated drug called Visudyne, which is administered intravenously and takes under 15 minutes to travel to the problematic blood vessels behind the eyes. A red
laser, directed onto that area for just a minute and a half, destroys these abnormal growths, while leaving healthy tissue intact.

In a clinical trial, 61.4 percent of those treated with Visudyne had vision which stabilized or improved, compared with 45.9 percent of patients in the control group. (This means that even in some individuals who got no treatment at all, vision did not worsen during that time period.) On the negative side: the photodynamic therapy cannot repair existing damage; the stabilization does not appear to be permanent; and it can be used only for 20 to 30 percent of those with the wet form of the disease. Nevertheless, it is an avenue that shows some promise and offers hope in a fairly bleak landscape. Another photodynamic drug for AMD is also currently in clinical trials.

Other treatments being studied include antiangiogenic drugs such as thalidomide, that inhibit the development of new blood vessels, and low dose radiation therapy. Zarbin's retinal team at the medical school is leading the way in another investigative area. They are working to perfect a technique that surgically removes the harmful blood vessels from the retina, and simultaneously, to address a cascade of events that can produce further damage to the eye. Sound relatively simple? The premise is, but the actuality is not.

Basically, the surgeon makes a tiny incision in the retina and pulls out the abnormal blood vessels, which eliminates the source of blood and fluid leakage. For patients whose disease has not caused permanent scarring and damage to the retina, this approach should work to curb further deterioration. But experience has shown that this technique only works for some of the people some of the time.

Why? There seem to be multiple reasons. At least some retinal pigment epithelium (RPE) cells- needed to maintain viable photoreceptors - are so closely entwined with the abnormal blood vessels that they are also excised in the process. And while it seems reasonable that other RPE cells would move into the spot and fill in the gap created by the surgery, this doesn't happen. "This area of the retina just seems to degenerate, even if
it was in decent shape before surgery, and central vision does not improve," Zarbin explains.

So the ophthalmological team is experimenting with several approaches aimed to better the outcome of surgery. RPE cell transplantation - an approach that works in animals, so should work for humans - is high on their list. The idea is to take the patient‘s own, functioning RPE cells from the periphery of the retina and move them into the central area where the blood vessels were removed and additional RPE cells are needed. Because the cells sometimes don‘t adhere to the site, Zarbin and Lucian Del Priore, MD, PhD, Chief of Vitreoretinal Surgery and co-director of the Center for Macular Degeneration Research and Treatment at NJMS, are experimenting with different techniques of harvesting and culturing these cells.

In other experiments, they are trying to stimulate the RPE cells to migrate from the healthy periphery of the retina into the center, either by altering the membrane surface with proteins that encourage cell migration or by stimulating the cells themselves with cytokines.

Chief among the researchers' problems is that no animal model exists for age-related macular degeneration, so they must rely on cadaver eyes from older donors in order to advance their work.

Although drug research and the hunt for additional genes promise some new therapies in the not-too-distant future, patients who already have advanced disease will probably not benefit. Surgery will most likely remain their best hope for treatment.

Even without a stunning treatment to reverse AMD, or to cure it, it's clear that those whose disease is caught early have more options for stopping the progressive loss of sight. If you're 55 or over, or even creeping toward that number, why not take the simple test printed below? It will be five minutes of your time well spent.

DO YOU HAVE SIGNS OF MACULAR DEGENERATION?

The Amsler Grid below is a chart that can reveal signs of wet macular degeneration. You can get one from your ophthalmologist and test your vision. Basically, the chart is a tool for monitoring your central vision. It makes it possible for you to tell if there are disturbances in your vision caused by changes in the retina. Here's how it works.

1. Sit in an area with good lighting and hold the chart at eye level at a comfortable distance. 2. If you wear glasses, keep them on, but cover one eye completely. 3. Stare with the other eye at the central dot on the grid. At the same time, observe the pattern of vertical and horizontal lines on the chart. 4. Repeat the test with the other eye. If you experience any of these changes, make an appointment with your opthalmologist immediately:

•Blurring ;

•Distortion or curvy lines ;

•Holes or spots in some areas of the grid




If you're concerned about the results or have questions, call your physician or the Macular Degeneration Center at NJMS at 973-972-2038.