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 patients 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 dont 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.
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