Project DetailsThis research investigates a method to slow the formation of ocular lipofuscin, a naturally occurring pigment soluble in fat and found in aging tissues. The development of lipofuscin correlates with the progression of various macular dystrophies and degenerations. As such, methods to halt or reverse the formation of ocular lipofuscin are highly sought after as means to better understand the link between lipofuscin and macular degenerations or dystrophies and as clinical interventions for their treatment. The objectives for our proposed research are to gather data in order to be able to proceed with a clinical trial designed to evaluate the extent to which C20-D3-vitamin A can impede the formation of ocular lipofuscin as well as to aid in the development of diagnostic methods to evaluate treatment compliance during the trial. This trial will help to determine the extent to which lipofuscin contributes to vision loss. The most innovative aspect of this research is that it involves a method to slow down the formation of ocular lipofuscin without interrupting the visual cycle or normal vitamin A metabolism, which can result in poor night vision. At the completion of our study, we anticipate that we will be able to: 1) determine whether treatment with C20-D3-vitamin A would be practical in humans; 2) evaluate the ability of C20-D3-vitamin A to slow lipofuscin formation in another animal model; 3) determine the time it would take for the vitamin to start working in order to better estimate proper dosing in future clinical studies; 4) evaluate whether urine analysis can be used as a potential method to measure treatment compliance in future clinical studies; and 5) elucidate how vitamin A is dynamically used in the body to promote vision and health.