Journal
CRITICAL REVIEWS IN TOXICOLOGY
Volume 42, Issue 7, Pages 613-632Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/10408444.2012.680431
Keywords
Parkinson's disease; rotenone; pathogenesis; dopaminergic neuron; neurodegeneration; mechanism
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Funding
- National Natural Science Foundation of China [30870866, 81071021, 31171211]
- Wuhan Science and Technology Bureau, China [20066002100]
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The etiology of Parkinson's disease (PD) is attributed to both environmental and genetic factors. The development of PD reportedly involves mitochondrial impairment, oxidative stress, a-synuclein aggregation, dysfunctional protein degradation, glutamate toxicity, calcium overloading, inflammation and loss of neurotrophic factors. Based on a link between mitochondrial dysfunction and pesticide exposure, many laboratories, including ours, have recently developed parkinsonian models by utilization of rotenone, a well-known mitochondrial complex I inhibitor. Rotenone models for PD appear to mimic most clinical features of idiopathic PD and recapitulate the slow and progressive loss of dopaminergic (DA) neurons and the Lewy body formation in the nigral-striatal system. Notably, potential human parkinsonian pathogenetic and pathophysiological mechanisms have been revealed through these models. In this review, we summarized various rotenone-based models for PD and discussed the implied etiology of and treatment for PD.
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