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From gene discovery to preventing eye disease in retinitis pigmentosa

nal injury that could be repaired over a period of weeks to months.

"It is tempting to speculate that extremely slow recovery of vision following light exposure observed in patients with rhodopsin mutations may represent the human equivalent of retinal repair mechanisms observed in the rhodopsin mutant dogs," says Cideciyan. "Better understanding of the components of this repair mechanism may lead to new treatment strategies based on augmentation of innate repair."

"The potentially damaging effects of environmental light have been well-studied and discussed in the past," adds Jacobson. "Now, we have clues that a specific subgroup of patients may be far more vulnerable to light than others. These patients should be identified clinically and by gene testing and then counseled about this vulnerability. A clinical trial is definitely indicated."

The research from the Penn-Cornell investigators ushers in a new era of eye-disease prevention by considering the interaction of genetics and environment in this case exposure to light on an individual basis. The investigators recommend that all patients with the clinical diagnosis of RP should see an RP specialist to determine their family pattern (the every generation or dominant form is the vulnerable one), their eye disease pattern by specialized (low-light level) testing, and the genetic cause of their RP to know whether this research applies to them and their family members.


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Contact: Olivia Fermano
olivia.fermano@uphs.upenn.edu
215-349-5653
University of Pennsylvania School of Medicine
22-Mar-2005


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