Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis
By C. Henchcliffe, M. Beal. Nature Clinical Practice Neurology, 2008
791 citations recorded by the source corpus.
Subfields: Molecular Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/ccdbc4808b54cc0facada0aac139432b623afbc9
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Citations in the corpus
- Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease (2012, background): “In particular, increased PD risk has been linked to mutations in α-synuclein, parkin, PINK1, DJ-1, and LRRK2, all of which have been related to mitochondria [136].”
- Metals, oxidative stress and neurodegenerative disorders (2010, positive): “Mutations in PINK1 (PTEN-induced putative kinase) gene are the second most common cause of autosomal recessive, early onset Parkinsonism following the parkin mutations [115].”
- Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “…pathways that converge at mitochondria (reviewed in Abou-Sleiman et al , 2006; Lin and Beal, 2006; Mandemakers et al , 2007; Bogaerts et al , 2008; Henchcliffe and Beal, 2008; Schapira, 2008; Vila et al , 2008; Van Laar and Berman, 2009; Bueler, 2010; Burbulla et al , 2010; Winklhofer and Haass,…”