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Genetic variants influencing retinal degeneration and neuroprotection in the eye
Light may a co-factor accelerating blinding retinal diseases in humans and visible light can directly damage the retina by inducing photoreceptor apoptosis. In rods, light damage is rhodopsin-mediated and correlates directly with the rate of rhodopsin regeneration in the visual cycle. A genetic variant in the Rpe65 gene influences the levels of the RPE65 protein that is essential for the regeneration of functional rhodopsin. High amounts of RPE65 correlate with fast regeneration kinetics and a high light damage susceptibility. Slowing the visual cycle by the Rpe65 variant or by the pharmacological application of halothane reduces or completely protects against light damage, respectively. The application of Dexamethasone or Erythropoietin also protects the retina. However, protection does not involve modulation of the visual cycle but rather interferes with intracellular molecular signaling pathways. Therefore, several targets exist in the neuroretina that may be aimed at to preserve vision in patients with blinding diseases.