A
Alexander Panov
Researcher at Mercer University
Publications - 32
Citations - 6727
Alexander Panov is an academic researcher from Mercer University. The author has contributed to research in topics: Mitochondrion & Oxidative stress. The author has an hindex of 18, co-authored 32 publications receiving 6334 citations. Previous affiliations of Alexander Panov include Russian Academy of Sciences & Carolinas Medical Center.
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Chronic systemic pesticide exposure reproduces features of Parkinson's disease
TL;DR: It is reported that chronic, systemic inhibition of complex I by the lipophilic pesticide, rotenone, causes highly selective nigrostriatal dopaminergic degeneration that is associated behaviorally with hypokinesia and rigidity.
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Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines
Alexander Panov,Claire-Anne Gutekunst,Blair R. Leavitt,Michael R. Hayden,James R. Burke,Warren J. Strittmatter,J. Timothy Greenamyre +6 more
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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An In Vitro Model of Parkinson's Disease: Linking Mitochondrial Impairment to Altered α-Synuclein Metabolism and Oxidative Damage
Todd B. Sherer,Ranjita Betarbet,Amy K. Stout,Serena Lund,Melisa J. Baptista,Alexander Panov,Mark R. Cookson,J. Timothy Greenamyre +7 more
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.
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Complex I and Parkinson's disease.
TL;DR: Chronic rotenone exposure accurately recapitulated the pathological, biochemical, and behavioral features of PD, suggesting relatively subtle complex I abnormalities‐‐either genetic or acquired‐‐may be central to the pathogenesis of PD.
Journal ArticleDOI
Mechanism of toxicity of pesticides acting at complex I: relevance to environmental etiologies of Parkinson’s disease
Todd B. Sherer,Jason R. Richardson,Claudia M. Testa,Byoung Boo Seo,Alexander Panov,Takao Yagi,Akemi Matsuno-Yagi,Gary W. Miller,J. Timothy Greenamyre,J. Timothy Greenamyre +9 more
TL;DR: Examination of in vitro toxicity and mechanism of action of several commercially used pesticides found that PYR was a more potent inhibitor of mitochondrial respiration and caused more oxidative damage than ROT, and suggest that further study is warranted into environmental agents that inhibit complex I for their potential role in PD.