Speaker
Description
Rod and cone photoreceptors are among the most metabolically active cells in the human body, relying on tightly regulated redox homeostasis to maintain function. In retinal degeneration resulting from chronic blue light exposure or inherited degenerative conditions such as retinitis pigmentosa (RP), the progressive loss of photoreceptors disrupts this balance, leading to an accumulation of reactive oxygen species (ROS) that accelerates further cell death. Two proteins produced by rod photoreceptors have emerged as promising therapeutic targets. The rod-derived cone viability factor (RdCVF) promotes cone survival by enhancing glucose uptake and supporting aerobic glycolysis. Its long isoform (RdCVFL) protects both rods and cones by regulating the redox environment. While the therapeutic potential of each protein has been investigated independently, their combined effect has not yet been examined in a unified mathematical framework. RdCVF and RdCVFL act on distinct but coupled biological processes, targeting metabolic support and oxidative stress regulation, respectively. A dual-intervention strategy may therefore offer substantially greater neuroprotection than either treatment alone. In this work, we develop and analyze an optimal control model incorporating both RdCVF and RdCVFL as co-administered treatments. This provides a mathematical basis for evaluating the synergistic potential of this dual-intervention approach in slowing or halting photoreceptor degeneration arising from chronic blue light exposure, RP, and related retinal diseases.
