Woodrow Wilson Undergraduate Research Fellowship Program
Johns Hopkins University
3400 N. Charles Street
Baltimore, MD 21218
Age-related macular degeneration (AMD), clinically characterized as wet and dry forms, is the leading cause of severe vision loss in patients over 50 in developed countries, with a current prevalence in the Unites States of 1.75 million and a predicted increase to 3 million by 2030. The pathology of AMD includes degeneration of retinal pigment epithelium (RPE) and photoreceptors, abnormal deposits of extracellular substances (e.g., drusen) and choroidal neovascularization (CNV), a growth of new blood vessels behind the retina that potentially leads to a disruption in central vision, etc. On the cellular level, it is the migration of activated retinal microglia, glial cells involved in the immune response, into the outer retina that is an important cause of AMD pathogenesis. The mechanisms underlying this migration appear to be at least partially regulated by chemokine signaling, such as C-X-C chemokine receptor (CXCR) 5, which appears to play a role in attracting retinal microglia to the outer retina. Better understanding of the role of CXCR5 in AMD pathogenesis, the identity of CXCR5 expressing cells, and the effects of CXCR5 inhibition on CNV development, would be useful for the identification of novel targets and the design of better agents for the treatment or prevention of AMD.