Retinitis pigmentosa can be slowed by reprogramming metabolism of photoreceptors, study shows
Columbia University Medical Center (CUMC) researchers have demonstrated that vision loss associated with a form of retinitis pigmentosa (RP) can be slowed dramatically by reprogramming the metabolism of photoreceptors, or light sensors, in the retina. The study, conducted in mice, represents a novel approach to the treatment of RP, in which the therapy aims to correct downstream metabolic aberrations of the disease rather than the underlying genetic defect.
The findings were published online today in the Journal of Clinical Investigation.
“Although gene therapy has shown promise in RP, it is complicated by the fact that defects in 67 genes have been linked to the disorder, and each genetic defect would require a different therapy,” said study leader Stephen H. Tsang, MD, PhD, the László Z. Bitó Associate Professor of Ophthalmology, Pathology and Cell Biology, and the Institute of Human Nutrition. “Our study shows that precision metabolic reprogramming can improve the survival and function of affected rods and cones in at least one type of RP. Since many, if not most, forms of the disorder have the same metabolic error, precision reprogramming could conceivably be applied to a wide range of RP patients.”
RP, an inherited form of vision loss, is caused by genetic defects that lead to the breakdown and loss of rods, the photoreceptors in the retina that enable peripheral and night vision. Over time, the deterioration of rods compromises the function of cones, the color-sensing photoreceptors. People with RP start to experience vision loss in childhood, and many are blind by the time they reach adulthood. Currently, there is no cure or effective treatment for RP, which affects about 1 in 4,000 people worldwide.
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Source: News Medical