Proteasomal function is impaired in substantia nigra in Parkinson's disease.
By K. McNaught, P. Jenner. Neuroscience Letters, 2001
663 citations recorded by the source corpus.
Subfields: Cell Biology, Neurology
View Paper: https://www.semanticscholar.org/paper/eab8203c6e6ed17ba935b5a72301cd76f91847ed
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Citations in the corpus
- Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease (2011, positive): “When a reduction in proteasomal catalytic activity and subunit expression in the SN in PD was reported, attempts to use this as a means of producing a new animal model of PD commenced (McNaught and Jenner, 2001; McNaught et al., 2002a).”
- Alpha-synuclein and neurodegenerative diseases (2001, background): “So, it has been shown that proteasomal function is impaired in the substantia nigra of PD patient”
- Expression of A53T Mutant But Not Wild-Type α-Synuclein in PC12 Cells Induces Alterations of the Ubiquitin-Dependent Degradation System, Loss of Dopamine Release, and Autophagic Cell Death (2001, background): “Copyright © 2001 Society for Neuroscience 0270-6474/01/219549-12$15.00/0 (Kitada et al., 1998; Leroy et al., 1998; Shimura et al., 2000; McNaught and Jenner, 2001; McNaught et al., 2001), and on the dopaminergic phenotype, because this seems to be affected out of proportion to the degree of…”
- Oxidative stress in Parkinson's disease (2003, background): “In addition, a substantial body of evidence now suggests that alterations in protein ubiquitination and protein degradation by the 26S proteasome may play a primary role in the pathogensis of PD.(23,24) Indeed, oxidative stress appears to form part of a cascade of biochemical changes that lead to do”
- Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases (2015, background): “P. (2002). Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson’s disease.”
- Parkinson disease: from pathology to molecular disease mechanisms. (2013, background): “Examination of the 26S proteasome in PD revealed selective changes in its catalytic activity and composition in the SNc that were associated, perhaps wrongly, with impaired degradation of a-synuclein [97,100,151].”
- Pathogenesis of parkinson's disease: dopamine, vesicles and α-synuclein (2002, background): “There is evidence that the UPP is also impaired in sporadic Parkinson's diseas”
- Diagnosis and treatment of Parkinson disease: molecules to medicine. (2006, background): “Additional evidence for the importance of the proteasome comes from pathologic studies that have found decreased proteasomal activity and expression in the SN of PD patients and the intriguing, but controversial, finding that exposure to proteasomal toxins can induce PD-like pathology in animal mode”
- Stages in the development of Parkinson’s disease-related pathology (2004, background): “The reason that the involved nerve cells are not able rapidly to eliminate the abnormal protein via ubiquitination and proteasomal recycling is still unclear (Trojanowski and Lee 2000; Chung et al. 2001; Ding and Keller 2001; McNaught and Jenner 2001; Walker and LeVine 2001).”