St. Louis, March 1, 1999 -- Investigators at Washington University School of Medicine in St. Louis have found that a mechanism key to immune-privilege in the eye also plays a role in age-related macular degeneration, the leading cause of blindness in people over the age of 60.
Reporting today in the March issue of Nature Medicine, the investigators link a form of macular degeneration to potential problems involving the interaction between two proteins called Fas and Fas ligand (FasL). Contact between these two molecules prevents immune system activity in the front of the eye. At the back of the eye in the retina, the interaction between Fas and FasL is involved in preventing growth of blood vessels that interfere with vision in the "wet" form of age-related macular degeneration. When one of these is deficient, vision loss can occur.
"There are two forms of the disease," said investigator Henry J. Kaplan, M.D. professor of ophthalmology and visual sciences at the School of Medicine. "The dry form is the more common type, but the wet form is associated with severe loss of vision. In the wet form of the disease, abnormal vessels grow beneath the retina and interfere with central vision. In the dry form, while there is vision loss, there are no unwanted vessels growing beneath the retina."
The vessels grow from the choroid, a structure beneath the retina. For 10 years, Kaplan and colleagues have attempted to surgically remove abnormal vessels and scar tissue. The limitation of this approach is that while removing the vessels, the surgeon also is likely to remove a thin layer of cells at the back of the retina called the retinal pigment epithelium (RPE). These cells nourish photoreceptor cells that convert light impulses into vision. If a surgeon removes abnormal vessels along with the RPE layer, the surgery probably will not restore vision.
The search for a different treatment for the disease led Kaplan, a
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Contact: Jim Dryden
dryden@medicine.wustl.edu
314-286-0110
Washington University School of Medicine
2-Mar-1999