Chronic systemic pesticide exposure reproduces features of Parkinson's disease

By R. Betarbet, T. Sherer, G. Mackenzie, M. Garcia-Osuna, A. Panov, J. Greenamyre. Nature Neuroscience, 2000

3,737 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/3e73a96b9a0ba2efdff53b044aa3b6be0844b858

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Elias K. Michaelis
2. Valina L. Dawson
3. T. Dawson
4. P. Jenner
5. S. Duty
6. M. Block
7. S. Przedborski
8. D. Dexter

In Neurology

1. R. Youle
2. Valina L. Dawson
3. T. Dawson
4. P. Jenner
5. Elias K. Michaelis
6. Derek P. Narendra
7. S. Jin
8. S. Duty

Citations in the corpus

• Molecular pathophysiology of Parkinson's disease. (2005, background): “…complex-I inhibitors such as rotenone and paraquat clearly lead to aggregation and accumulation of α-synuclein in vitro and in animal models (Betarbet et al. 2000; Manning- Bog et al. 2002; Sherer et al. 2002b, 2003), and other forms of oxidative and nitrosative stress also promote…”
• Mitochondrial dysfunction and molecular pathways of disease. (2007, background): “Complex I is especially susceptible to nitric oxide (NO) damage, and animals administered natural and synthetic complex I antagonists have undergone death of neurons (Dauer and Przedborski, 2003; Betarbet et al., 2000; Qi et al., 2003 ).”
• ER stress and neurodegenerative diseases (2006, background): “Environmental factors, such as pesticides and other conditions have been suggested to cause sporadic PD, which constitutes more than 90% of the patients.(29,31) Recent studies discussed below indicate that also ER stress in conjunction with abnormal protein degradation can contribute to the pathophy”
• PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin (2010, background): “parkinsonian syndrome in humans and animal models [9,10].”
• An In Vitro Model of Parkinson's Disease: Linking Mitochondrial Impairment to Altered α-Synuclein Metabolism and Oxidative Damage (2002, background): “Rotenone is also a well characterized, specific inhibitor of complex I. Chronic systemic rotenone exposure reproduced many features of PD, including nigrostriatal dopaminergic lesions and development of -synuclein-positive cytoplasmic inclusions in nigral neurons (Betarbet et al., 2000).”
• Generation of reactive oxygen species by the mitochondrial electron transport chain (2002, background): “While the physiological and pathological significance of anti-mycin A-induced ROS production at complex III is not clear, there is ample evidence that ROS production at complex I is important in the pathogenesis of Parkinson’s disease and other mitochondrial diseases related to complex I deficiencie”
• Endoplasmic Reticulum Stress and the Unfolded Protein Response in Cellular Models of Parkinson's Disease (2002, background): “…with additional drug-induced models for PD. MPP and rotenone are mitochondrial inhibitors that cause selective degeneration of nigrostriatal neurons in vivo (Langston et al., 1983; Betarbet et al., 2000) and death of dopaminergic neurons and neuronal PC12 cells in vitro (Seaton et al., 1997).”
• Oxidative stress and nitration in neurodegeneration: cause, effect, or association? (2003, background): “Chronic administration of the mitochondrial electron-transport inhibitor rotenone was reported to recapitulate features of Parkinson disease in rats, including α-synuclein inclusions (50).”
• Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease (2011, background): “The best known of the models to emerge from this is the rotenone model of PD, but British Journal of Pharmacology (2011) 164 1357–1391 1367 since its first introduction (Betarbet et al., 2000), it has continued to provoke much debate (e.g. Cicchetti et al., 2009; Greenamyre et al., 2010).”