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Gene Linked to 'Dry' Macular Degeneration
Date:8/27/2008

Unfortunately, the treatment appears to simultaneously activate TLR3 -- resulting in a 60 percent spike in retinal cell death among mice and humans genetically susceptible to developing dry AMD. The result: RNAi may help protect against wet AMD while boosting the risk for dry AMD, the study authors said.

"This raises particular concerns regarding RNAi therapy for wet AMD," Zhang said. "But by establishing this link between the treatment for the wet form of AMD and the potential harmful effect on the dry form of the disease, we can perhaps better understand the mechanisms of both diseases."

Age-related macular degeneration is the leading cause of blindness in adults over the age of 60, according to the U.S. National Eye Institute. The progressively worsening disease affects the macula portion of the eye, located in the center of the retina, which enables detailed vision.

The disease can strike in two ways: wet and dry. In its wet form --sometimes referred to as "advanced AMD" -- loss of vision occurs rapidly due to the growth of abnormal blood vessels under the macula, leading to leakage of blood and fluids. In its more slowly progressing dry form, light-sensitive macular cells begin to break down, leading to a blurring of vision in one or both eyes, according to the eye institute.

Addressing the new findings, Rando Allikmets, a professor of ophthalmology, pathology and cell biology at Columbia University, urged restraint.

"I think these results have to be taken with caution, because the association effect of TLR3 with AMD is very small when compared to the disease's association with some other genes," he said. "And there has been already one study saying there is absolutely no association of the TLR3 genetic variant with AMD. So, this raises a question and a need for further edification. It could be that this is just a spurious finding, and there is, in fact, no association with AMD."

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