Subcutaneous rotenone exposure causes highly selective dopaminergic degeneration and alpha-synuclein aggregation.

By Todd B. Sherer, Jin-ho Kim, R. Betarbet, J. Greenamyre. Experimental Neurology, 2003

748 citations recorded by the source corpus.

Subfields: Neurology

View Paper: https://www.semanticscholar.org/paper/72896a2d1c5e4ae118e8c1613226317ec1aa5c2a

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In Neurology

1. P. Jenner
2. Valina L. Dawson
3. T. Dawson
4. S. Duty
5. D. Selkoe
6. S. Przedborski
7. J. Bové
8. C. Perier

Citations in the corpus

• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “In vivo studies with rats also demonstrated alpha-synuclein aggregation following systemic exposure to the pesticides rotenone [234] or dichlorvos [235].”
• Cell biology of protein misfolding: The examples of Alzheimer's and Parkinson's diseases (2004, background): “Although normally a 'natively unfolded' soluble protein, α-synculein forms amyloid-like filaments under certain conditions that include mitochondrial complex I deficienc”
• Toxin-induced models of Parkinson’s disease (2005, background): “In contrast to the 6-OHDA and MPTP models, in rotenone-infused rats, some of the remaining substantia nigra dopaminergic neurons contain proteinaceous inclusions.(91,109,110) Like LBs in PD, these inclusions are immunoreactive for both ubiquitin and -synuclein,(91) and by electron microscopy they ap”
• Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease (2011, background): “The outcome appears just as variable when rotenone is given by subcutaneous, rather than intravenous infusion (Sherer et al., 2003c; Lapointe et al., 2004), casting doubt upon the reproducibility of these rotenone models for use in drug discovery programmes.”
• Molecular pathophysiology of Parkinson's disease. (2005, background): “…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 α-synuclein aggregation (Ischiropoulos & Beckman 2003).”
• Mechanism of Toxicity in Rotenone Models of Parkinson's Disease (2003, methodology): “Exposure of rats to the pesticide and complex I inhibitor rotenone reproduces features of Parkinson’s disease, including selective nigrostriatal dopaminergic degeneration and -synuclein-positive cytoplasmic inclusions (Betarbet et al., 2000; Sherer et al., 2003).”
• A highly reproducible rotenone model of Parkinson's disease (2009, background): “As described with intravenous and subcutaneous administration of rotenone by osmotic pump, we have found that intraperitoneal rotenone also causes α-synuclein accumulation and aggregation in substantia nigra (Betarbet et al., 2006; Betarbet et al., 2000; Sherer et al., 2003).”
• Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases (2015, background): “Rotenone has also the capacity to activate microglia (Sherer et al., 2003); Gao et al.”
• Oxidative Stress in Parkinson's Disease: A Mechanism of Pathogenic and Therapeutic Significance (2008, background): “Rotenone, a complex I inhibitor induces dopaminergic cell loss in cell culture [32] and can cause PD type neuropathology and movement abnormalities [33-35].”