Descriptor of Research
Our laboratory studies mechanisms causing diabetic retinopathy with specific focus on damage to the neural retina, an early event in the pathogenesis of disease. Our hypothesis is that diabetes-induced metabolic dysfunction primarily injures the neural retina, a highly metabolically-active tissue, and that the retinal microvasculature is only secondarily damaged due to its dependence on neurons and glia for trophic support. Our goals are to uncover novel approaches to both therapy and early diagnosis of diabetic retinopathy. In our current approach, we are identifying abnormalities of lipid metabolism in the diabetic retina and their contribution to vision loss. We utilize a wide variety of mouse models, reflective of human type 1 and type 2 diabetes mellitus, to determine how such abnormalities alter the physiology of the neural retina. We also use these models to test treatment strategies that could exploit pathways related to lipid processing, with the potential to be more effective than conventional therapy when applied at the neural stage of disease. In addition to our animal studies, we are involved a number of studies in patients with diabetic retinopathy, with an emphasis on early detection of disease using functional measures.