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J. Timothy Greenamyre

Researcher at University of Pittsburgh

Publications -  165
Citations -  20052

J. Timothy Greenamyre is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Parkinson's disease & Neurodegeneration. The author has an hindex of 65, co-authored 160 publications receiving 18134 citations. Previous affiliations of J. Timothy Greenamyre include Veterans Health Administration & University of Texas Southwestern Medical Center.

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Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines

TL;DR: It is shown that lymphoblast mitochondria from patients with HD have a lower membrane potential and depolarize at lower calcium loads than do mitochondriaFrom controls, and mitochondrial calcium abnormalities occur early in HD pathogenesis and may be a direct effect of mutant huntingtin on the organelle.
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Mechanism of toxicity in rotenone models of Parkinson's disease.

TL;DR: The involvement of oxidative damage in rotenone toxicity is demonstrated and antioxidant therapies for Parkinson's disease are supported, using three model systems of increasing complexity.
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Subcutaneous Rotenone Exposure Causes Highly Selective Dopaminergic Degeneration and α-Synuclein Aggregation

TL;DR: It is demonstrated that chronic systemic exposure to the pesticide and mitochondrial toxin rotenone through jugular vein cannulation reproduced many features of Parkinson's disease in rats, including nigrostriatal dopaminergic degeneration and formation of alpha-synuclein-positive cytoplasmic inclusions in nigral neurons.
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A highly reproducible rotenone model of Parkinson's disease

TL;DR: This version of the rotenone model of Parkinson's disease is highly reproducible and may provide an excellent tool to test new neuroprotective strategies.
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An In Vitro Model of Parkinson's Disease: Linking Mitochondrial Impairment to Altered α-Synuclein Metabolism and Oxidative Damage

TL;DR: These studies indicate that chronic low-grade complex I inhibition caused by rotenone exposure induces accumulation and aggregation of α-synuclein and ubiquitin, progressive oxidative damage, and caspase-dependent death, mechanisms that may be central to PD pathogenesis.