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Etiology and pathogenesis of Parkinson's disease
Schapira AH, Jenner P.. Movement disorders : official journal of the Movement Disorder Society, 2011-05-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
The past 25 years have seen a major expansion of knowledge concerning the cause of Parkinson's disease provided by an understanding of environmental and genetic factors that underlie the loss of nigral dopaminergic neurons. Based on the actions of toxins, postmortem investigations, and gene defects responsible for familial Parkinson's disease, there is now a general consensus about the mechanisms of cell death that contribute to neuronal loss in Parkinson's disease. Mitochondrial dysfunction, oxidative stress, altered protein handling, and inflammatory change are considered to lead to cell dysfunction and death by apoptosis or autophagy. Ageing is the single most important risk factor for Parkinson's disease, and the biochemical changes that are a consequence of aging amplify these abnormalities in Parkinson's disease brain. What remains to be determined is the combination and sequence of events leading to cell death and whether this is identical in all brain regions where pathology occurs and in all individuals with Parkinson's disease. Focusing on those events that characterize Parkinson's disease, namely, mitochondrial dysfunction and Lewy body formation, may be the key to further advancing the understanding of pathogenesis and to taking these mechanisms forward as a means of defining targets for neuroprotection.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Schapira, A. H., & Jenner, P. (2011). Etiology and pathogenesis of Parkinson's disease. Movement disorders : official journal of the Movement Disorder Society. https://doi.org/10.1002/mds.23732
Vancouver
Schapira AH, Jenner P. Etiology and pathogenesis of Parkinson's disease. Movement disorders : official journal of the Movement Disorder Society. 2011. doi:10.1002/mds.23732. PMID: 21626550.
BibTeX
@article{schapira2011-21626550,
author = {Schapira, A. H. and Jenner, P.},
title = {{Etiology and pathogenesis of Parkinson's disease}},
journal = {Movement disorders : official journal of the Movement Disorder Society},
year = {2011},
doi = {10.1002/mds.23732},
pmid = {21626550},
url = {https://doi.org/10.1002/mds.23732}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Based on the actions of toxins, postmortem investigations, and gene defects responsible for familial Parkinson's disease, there is now a general consensus about the mechanisms of cell death that contribute to neuronal loss in Parkinson's disease.
- Mitochondrial dysfunction, oxidative stress, altered protein handling, and inflammatory change are considered to lead to cell dysfunction and death by apoptosis or autophagy.
- Ageing is the single most important risk factor for Parkinson's disease, and the biochemical changes that are a consequence of aging amplify these abnormalities in Parkinson's disease brain.
- What remains to be determined is the combination and sequence of events leading to cell death and whether this is identical in all brain regions where pathology occurs and in all individuals with Parkinson's disease.
- Focusing on those events that characterize Parkinson's disease, namely, mitochondrial dysfunction and Lewy body formation, may be the key to further advancing the understanding of pathogenesis and to taking these mechanisms forward as a means of defining targets for neuroprotection.
Why it matters
This review states that mitochondrial dysfunction, oxidative stress, altered protein handling and inflammation are thought to lead to cell dysfunction and death in Parkinson's disease, with ageing the most important risk factor. It discusses possible targets for neuroprotection but reports no treatment or cure.
Study details
- Evidence strengthLow
How this study scored 49/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Movement disorders : official journal of the Movement Disorder Society) |
| Journal's citation record | 3 / 4 | Movement Disorders: journal h-index 281 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2011 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 659 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 38.8 citations a year over 17 year(s) since 2011 |
| Impact for its field and year | 5 / 6 | Cited 29.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 3 / 4 | Cited 108 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Peter Jenner: h-index 71 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 21626550) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 49 / 100 | — |
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