Altered proteasomal function in sporadic Parkinson's disease.

By Kevin St, Mcnaught, R. Belizaire, O. Isacson, P. Jenner, W. Olanow. Experimental Neurology, 2003

620 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/38d055c687e7b07d30aa299b0930f58e154e421d

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Citations in the corpus

Molecular pathophysiology of Parkinson's disease. (2005, background): “Consis - tent with this notion there are both struc - tural and functional deficits in the 20 / 26S pro - teasome in the SNc of sporadic PD patients ( McNaught et al .”
The roles of intracellular protein-degradation pathways in neurodegeneration (2006, background): “These include sporadic PD, in which levels of 20/26S proteasomes and proteasome activity are reduced in vulnerable regions, and H”
Etiology and pathogenesis of Parkinson's disease (2011, background): “There is a reduction in proteasomal enzyme activity in the substantia nigra that is specific for PD and does not occur in other areas of the brain.(70,71) In addition, there are alterations in the expression of proteasomal subunits and in their regulatory caps that lead to the concept of a different”
The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “In the SNpc of PD patients, evidence has been presented for impaired UPS with structural proteasome alterations including loss of the alpha-subunit, the component that regulates and stabilizes the proteasome complex ([165, 166].”
Aggregated α‐synuclein activates microglia: a process leading to disease progression in Parkinson's disease (2005, background): “It is believed that missense mutations (A30P (19), A53T (20), and, more recently, E46K (21)) or overexpression of the -synuclein gene (22) and -synuclein damaged during the aging process or environmental exposure (reviewed in ref 23) appear to contribute at least partially to familial and sporadic P”
Dopamine covalently modifies and functionally inactivates parkin (2005, background): “Because thioester formation is crucial to the molecular machinery that mediates polyubiquitination and protein degradation, we propose that the ability of dopamine to functionally inactivate proteins such as parkin and UbcH7 could partially explain the reported decrease in the proteasomal activity i”
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”