Madilyn Stahl

Age-related macular degeneration (AMD) is the leading cause of blindness in the elderly. AMD is characterized by the loss of the retinal pigment epithelium (RPE) cells, which are essential for maintaining normal function of photoreceptors in the retina. Previous studies of human donors with AMD show that the RPE mitochondrial defects are a key event in AMD pathology. Evidence includes increased mtDNA damage and altered content of mitochondrial proteins in donors with AMD. Additionally, mitochondrial OXPHOS (oxidative phosphorylation) activity is decreased in cultured RPE from AMD donors. The hypothesis is that these defects are due in part to reduced content of mitochondria in diseased RPE. In this study, human donor RPE with (n = 76) or without (n = 39) AMD were used to evaluate the mitochondrial content per cell. Quantitative PCR (qPCR) was utilized to assess the total mitochondria copies per RPE cell, and western blotting was used to measure mitochondrial content per cell. The proteins studied are part of the electron transport chain (ETC), a component of OXPHOS. This study found no significant change in mtDNA content in donors with AMD and no significant change in the amount of mitochondrial complexes in the ETC in donors with AMD. Therefore, mitochondrial defects associated with AMD are not due to reduced mitochondrial content.