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Gene Expression Responses in a Cellular Model of Parkinson's Disease

Brill II, Louis Beverly
Thesis/Dissertation; Online
Brill II, Louis Beverly
This research represents initial steps towards understanding the relation between changes in gene expression, mitochondrial function and cell death in cell-based models of Parkinson's disease. The main hypothesis is that rapid gene expression changes in cells exposed to parkinsonian neurotoxins occur, are dependent on mitochondrial status, and directly impact intracellular signaling pathways that determine whether a cell lives or dies. Our cellular model is comprised of SH-SY5Y neuroblastoma cells exposed to the parkinsonian neurotoxin methylpyridinium ion. Transcriptomic changes are evaluated with nylon and glass-based cDNA microarray technology. Cardinal symptoms of Parkinson's disease, characteristic pathological changes, therapeutic modalities, and current theories on the etiology of the disorder are discussed. Our results verify the existence of mitochondrial-nuclear signaling in the context of electron transport chain deficits, as well as suggesting the vital roles played in this process by previously described intracellular signaling pathways. These results will serve to direct future investigations into gene expression changes relevant to the processes of cell death and cell survival in our cellular model of Parkinson's disease, and may provide important insights into the pathophysiology of the in vivo disease process. Note: Abstract extracted from PDF text
University of Virginia, Department of Cell Biology, PHD (Doctor of Philosophy), 2004
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PHD (Doctor of Philosophy)
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