The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
The pathogenesis of cell death in Parkinson's disease
Abstract
A number of factors have been implicated in the pathogenesis of cell death in Parkinson's disease (PD). These include oxidative stress, mitochondrial dysfunction, inflammation, excitotoxicity, and apoptosis. While the precise pathogenic mechanism leading to neurodegeneration in PD is not known, there is considerable evidence suggesting that cell death occurs by way of a signal-mediated apoptotic process. PD is also characterized by intracellular proteinaceous inclusions or Lewy bodies. Proteolytic stress arises as a consequence of the excessive production of misfolded proteins, which exceed the capacity of the ubiquitin-proteasome system to degrade them. Recent genetic and laboratory studies support the possible relevance of proteolytic stress to both familial and sporadic forms of PD. Postmortem studies have shown that in the SNc of sporadic PD patients there are reduced levels of the alpha subunit of the 20S proteasome and reduced proteolytic enzyme activities. A determination as to the precise cause of cell death in PD, and the identification of specific targets for the development of drugs that might modify disease progression is one of the most critical goals in PD research. It is anticipated that over the next few years there will be a flurry of scientific activity examining the mechanism of cell death and putative neuroprotective interventions.
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Cites
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Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
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Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
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Self-citationProtein degradation and protection against misfolded or damaged proteins.
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α-synuclein locus duplication as a cause of familial Parkinson's disease
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Cited by
The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
Parkinson disease: from pathology to molecular disease mechanisms
Dexter, D. T., & Jenner, P. (2013) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2013.01.018 · Cited by 707
Self-citationBuendia, I., Michalska, P., Navarro, E., Gameiro, I., Egea, J., & León, R. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2015.11.003 · Cited by 678
ROS and Brain Diseases: The Good, the Bad, and the Ugly
Popa-Wagner, A., Mitran, S., Sivanesan, S., Chang, E., & Buga, A.-M. (2013) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2013/963520 · Cited by 427
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Metadata
- Authors
- Jenner, P., & Olanow, C. W.
- Venue
- Neurology
- Published
- 2006-05-23
- Volume
- 66
- Issue
- 10_suppl_4
- Pages
- S24-36
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2082298489
- Cited by
- 446
- References
- 35
- FWCI
- 19.87
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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