Findings could lead to new treatments or even a cure, researchers say
TUESDAY, Sept. 22 (HealthDay News) -- Gene variants on chromosome 2 are associated with glaucoma in blacks, say researchers who studied 129 patients with the vision-robbing disease.
The finding may lead to new treatments or a cure, the scientists added.
Glaucoma is the leading cause of blindness among blacks, affecting close to 5 percent of the population. There is no cure or way to reverse glaucoma, which causes the gradual and irreversible loss of peripheral vision. But reducing intra-ocular pressure can slow the progression to blindness.
"The cause and progression of glaucoma are poorly understood, although we know there is a strong genetic predisposition to the disease," study co-author Dr. Robert N. Weinreb, director of the Hamilton Glaucoma Center and a professor of ophthalmology at the University of California, San Diego, said in a school news release.
This study included people in Barbados, where the incidence of glaucoma is nearly 10 percent (double the overall rate for blacks) because of a strong genetic influence.
"We have now identified very common gene variants that have a dramatic impact on an individual's risk for developing glaucoma," Dr. Kang Zhang, director of the Institute for Genomic Medicine and a professor of ophthalmology and human genetics at the Shiley Eye Center at UCSD, said in the news release.
"These gene variants are present in 40 percent of individuals with glaucoma in the Barbados population and explains nearly one-third of their genetic risk for the disease. This study should give us a better handle on earlier diagnoses and new therapies," Zhang said.
"Once we understand the specific gene or protein structure that is altered in the disease, we are one step closer to developing gene or stem cell-based therapies to treat glaucoma," Zhang noted.
The study appears in this week's online issue of the Proceedings of the National Academy of Sciences.
The U.S. National Eye Institute has more about glaucoma.
-- Robert Preidt
SOURCE: University of California, San Diego, news release, Sept. 21, 2009
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