Summary

Current evidence supports the hypothesis that inherent age-dependent losses in the retinal pigmented epithelium's capacity to maintain, repair, and regenerate contributes to the onset and progression of AMD. Cell type is determined, in large part, by modification of DNA and chromatin. This proposal seeks to determine whether age-dependent changes in DNA methylation can explain the age-related decline in retinal pigmented epithelium function.

Project Details

Changes in retinal pigment epithelium (RPE) cells due to age and environmental stress may be associated with the onset and progression of age‐related macular degeneration (AMD). These pressures can cause changes in gene activity and cell health through a process called epigenetics. This process, where genes are either activated or inactivated by the addition of specialized chemical groups to the DNA, occurs naturally during development and plays a key role in the determination of cellular function. Dr. Monte Radeke and collaborators will determine if changes to the original epigenetic programming of RPE can help explain the damage observed in AMD. They will use a state‐of‐the-art global analytical method to identify genes in both cultured RPE cells and human donor RPE whose epigenetic programming becomes altered with increasing age. If aging does cause epigenetic changes to genes in RPE cells, this research could lead to new treatments for AMD.