Glycolysis is the process by which our bodies generate energy by converting glucose into pyruvate. In the retina, glycolysis converts glucose into lactate, which supports energy needs in the retinal cells.
In this study, researchers at the University of Florida’s Department of Ophthalmology artificially increased the production of lactate using a modified protein called arrestin1 (ArrGG). This protein was packaged and delivered to the retina via adeno-associated virus (AAV), with a successful 25% increase in lactate secretion. This resulted in significant preservation of photoreceptors in a mouse retinal degeneration model.
What this means for Usher syndrome: These results demonstrate that increased glycolysis and lactate production via a modified arrestin1 protein may be a potential gene-agnostic therapeutic approach to slow down retinal degradation.
