An In Vitro Model of Parkinson's Disease: Linking Mitochondrial Impairment to Altered α-Synuclein Metabolism and Oxidative Damage

By T. Sherer, A. Stout, M. Baptista, A. Panov, M. Cookson, R. Betarbet, S. Lund, T. Greenamyre. Journal of Neuroscience, 2002

606 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/daf97c520634bba291f59e5782437ceb4a237f8c

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In Cellular and Molecular Neuroscience

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Citations in the corpus

Mitochondria in health and disease: perspectives on a new mitochondrial biology. (2004, background): “What does seem extraordinary is that the systemic administration of low doses of rotenone to rats seems to cause a PD like syndrome which includes the selective degeneration nigrostriatal neurons and the appearance of synuclein rich inclusion bodies which are a feature of the disease (Betarbet et al”
Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases (2015, background): “These effects were also observed in neuroblastoma SK-N-MC cells treated with rotenone (5 nM/4 weeks), as well as a loss of GSH, oxidative DNA and protein damage and caspase-dependent death (Sherer et al., 2002; Betarbet et al., 2006).”
Parkinson's Disease Mechanisms and Models (2003, background): “Nevertheless, this model was the first to link an environmental toxin of possible relevance to PD to the pathologic hallmark of -synuclein aggregation, an association also seen in cell culture studies (Uversky et al., 2001; Sherer et al., 2002; Lee et al., 2002a).”
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).”
Calcium and neurodegeneration (2007, background): “Chronic inhibition of mitochondrial complex I results in aggregation of α-synuclein, which is associated with apoptosis of neural cells (Sherer et al., 2002).”
Mechanism of Toxicity in Rotenone Models of Parkinson's Disease (2003, methodology): “The etiology of PD is not completely understood, but it is believed to involve an interaction between genetic and environmental factors (Sherer et al., 2002a).”
Cell-Produced α-Synuclein Is Secreted in a Calcium-Dependent Manner by Exosomes and Impacts Neuronal Survival (2010, background): “Cellular stressors do not lead to alterations of -synuclein secretion Oxidative stress has been shown to increase -synuclein levels and apoptosis in a variety of cell models (Sherer et al., 2002).”
Trends in oxidative aging theories. (2007, background): “…opposition to what one observes in mammals (and even in Drosophila), where partial inhibition of the mitochondrial electron transport chain (either by mutations or pharmacology) leads to a host of severe pathologies including myopathy and encephalopathy [92] [93] and Parkinsonism [94] [95] [96].”