Abstract
AMD is both the most prevalent disease with a CNS neurodegeneration and the most approachable due to the precision and in vivo visibility of photoreceptors and their support cells and very large biological effects. We hypothesize that a center of cone resilience due to xanthophyll carotenoids in foveal Müller glia overlies a larger surround of rod vulnerability due to age-related lipidization of Bruch’s membrane and choriocapillary endothelium degeneration. A timeline of disease progression is in view for drusen-driven disease, across the lifespan and aligning spatially on the biology of foveal cone vision. Rods elucidate the next chapter of deposit-driven AMD end-stages as well as a new neuroscience for lysosome-related organelles in the retinal pigment epithelium.