Lori Buhlman, Ph.D.

My lab team's overarching research goal is to elucidate mechanisms by which absence of the parkin protein causes a subset of human dopaminergic neurons to degenerate. Parkin loss-of-function Drosophilae are a particularly useful model in this context because the fruit fly has a brain region that is evolutionarily and functionally homologous to the brain structure that degenerates in Parkinson's disease patients. Parkin-null flies have selective degeneration in this region and subsequent motor deficits that are easily observed. We were the first to report deficits in a heterozygous parkin loss-of-function model. Using transgenic flies that facilitate visualization of mitochondria and autophagosomes in vulnerable fly neurons, we have reported significant differences in mitochondrial protein oxidation, morphology, and turnover in degenerating parkin-null fly neurons; these differences were not observed in similar but non-degenerating neurons. Our recent reports and current efforts are aimed at highlighting triggering sources of mitochondrial protein oxidation and testing novel Mn porphyrin antioxidants in our model.