Michigan State University | 1999 | B.S.
About
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 Drosophila is 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 undergoes degeneration 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 ex vivo, 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.
Title
Professor
Campus
Glendale, AZ
College
College of Graduate Studies - AZ
College of Veterinary Medicine
Department
Biomedical Sciences
Program
Biomedical Sciences (M.A.)
Biomedical Sciences (M.B.S.)
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Education
Michigan State University | 1999 | B.S.
Courses Taught
Molecular Cell Biology
Pharmacology I
Neuroscience
Application of Precision Medicine to Neurological Diseases
Publications
Organizations
Society for Neuroscience