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The overarching goal of this proposal is to determine whether altering lipid metabolism can decrease the burden of lipid-rich deposits (drusen).

Millions of Americans currently suffer from age-related macular degeneration (AMD), the most common cause of irreversible vision loss among older adults. With age, insoluble aggregates accumulate above and beneath the retinal pigment epithelium (RPE), the tissue that nourishes and supports the photoreceptors, the light-sensing cells of the eye. Over a lifetime, these aggregates conspire with environmental and genetic factors to damage the pigment epithelium and lead to a chronic decline in central focused vision (ie, the type of vision supported by the macula). Our work seeks to understand how these aggregates form, how they impact cell function, and whether a promising treatment strategy recently identified by our group will help prevent the formation of these aggregates and preserve healthy vision.  

This project uses data from a number of large studies to test whether limiting carbohydrates reduces risk of developing AMD

We are pursuing the combined goals of understanding the role and impact of CCR3 function during blood vessel development in the eye. Further, we are exploiting CCR3 to create images of the earliest stages of neovascular, ‘wet’, age-related macular degeneration (AMD). We are achieving this by using multiple molecular, biological, and genetic approaches. The potential impact of this proposal is very high as it will further define the functional relevance of the CCR3/eotaxin “axis” to the clinical development and progression of AMD. This will lead to the development of novel CCR3-targeting diagnostic and therapeutic strategies that can be used in the clinic to detect the subclinical stages of neovascular AMD, thus preventing this disease from progressing into a vision threatening state.

This project will measure the short-term cellular changes that occur prior to irreversible retinal atrophy in people with pentosan polysulfate sodium toxicity.