Age-related macular degeneration (AMD) is the leading cause of irreversible blindness in individuals over age 55 in the United States. Basic and clinical studies implicate the retinal pigment epithelium (RPE) as a primary site of pathology in the disease. Our research over the years has centered on antioxidative mechanisms in RPE and the retina and preventive modalities of retinal dysfunction in ocular diseases. These investigations use newer models of experimental AMD and have generated novel therapeutic approaches for the prevention of atrophic and neovascular AMD in particular with novel elastin like nanoparticles of endogenous and exogenous substrates.
Our focus has been on the role of specific and novel mitochondrial peptides (alphaB crystallin chaperone, humanin, and HM 10/10) in ameliorating mitochondrial dysfunction in oxidative injury to RPE and neural retina. Our new and recent research emphasis is on the mechanisms of deposition of oxidized lipids and lipoproteins via oxidative stress and complement activation in the pathophysiology of the choroid mouse models of lipoprotein deficiency and devising therapeutic approaches. Our lab is also actively engaged in research on the emerging role of senescence in AMD and in the development of novel senolytic drugs.
Key areas: Oxidative stress, antioxidant defense, membrane transporters, mitochondrial function, retinal pigment epithelium, age related macular degeneration (AMD), senescence, nanotherapy