Mitochondrial Mechanisms of Toxicant Induced Dopaminergic Neurodegeneration in C. elegans

Parkinson's Disease is the 2nd most prevalent neurodegenerative disease, and over 80% of cases cannot be attributed to genetic or familial causes. Many of these cases are likely the result of environmental exposures, including known associations with several pesticides and mitochondrial poisons, that result in the death of dopaminergic neurons. With over 300,000 synthetic chemicals registered for use, it's critical to develop the ability to rapidly screen these chemicals for their ability to damage dopamine neurons, and to learn the mechanism by which they do it to move towards prevention and facilitate early intervention and identify other interactions such as diet that contribute to pathological outcome. Here, we have developed a screening pipeline in the model organism C. elegans to support medium throughput, inexpensive screening. We have used these tools to investigate the bioenergetic versus redox contributions of complex I inhibitors to neurodegeneration and assessed the impact of high sugar diets on susceptibility to toxicant induced neurodegeneration.

Kate is a 5th year PhD Candidate in the Integrated Toxicology and Environmental Health Program at Duke University working in Dr. Joel Meyer's lab. Her research focuses on how mitochondrial toxicants induce Parkinson's Disease (PD), the 2nd most common neurodegenerative disease. Her thesis includes work using the model organism C. elegans to screen mitochondrial toxicants, investigating the mechanism by which electron transport chain Complex I inhibitors induce dopaminergic neurodegeneration, and how toxicant models of PD interact with diet. Kate earned her BS in Biochemistry and BA in Political Science as well as a Minor in Chemistry at Virginia Polytechnic Institute and State University in 2019.

THIS IS A HYBRID SEMINAR: In person and online via Zoom
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