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Oxidative stress and the pathogenesis of Parkinson's disease
Jenner P, Olanow CW.. Neurology, 1996-12-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Current concepts of the pathogenesis of Parkinson's disease (PD) center on the formation of reactive oxygen species and the onset of oxidative stress leading to oxidative damage to substantia nigra pars compacta. Extensive postmortem studies have provided evidence to support the involvement of oxidative stress in the pathogenesis of PD; in particular, these include alterations in brain iron content, impaired mitochondrial function, alterations in the antioxidant protective systems (most notably superoxide dismutase [SOD] and reduced glutathione [GSH]), and evidence of oxidative damage to lipids, proteins, and DNA. Iron can induce oxidative stress, and intranigral injections have been shown to induce a model of progressive parkinsonism. A loss of GSH is associated with incidental Lewy body disease and may represent the earliest biochemical marker of nigral cell loss. GSH depletion alone may not result in damage to nigral neurons but may increase susceptibility to subsequent toxic or free radical exposure. The nature of the free radical species responsible for cell death in PD remains unknown, but there is evidence of involvement of hydroxyl radical (OH.), peroxynitrite, and nitric oxide. Indeed, OH. and peroxynitrite formation may be critically dependent on nitric oxide formation. Central to many of the processes involved in oxidative stress and oxidative damage in PD are the actions of monoamine oxidase-B (MAO-B). MAO-B is essential for the activation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine to 1-methyl-4-phenylpyridinium ion, for a component of the enzymatic conversion of dopamine to hydrogen peroxide (H2O2), and for the activation of other potential toxins such as isoquinolines and beta-carbolines. Thus, the inhibition of MAO-B by drugs such as selegiline may protect against activation of some toxins and free radicals formed from the MAO-B oxidation of dopamine. In addition, selegiline may act through a mechanism unrelated to MAO-B to increase neurotrophic factor activity and upregulate molecules such as glutathione, SOD, catalase, and BCL-2 protein, which protect against oxidant stress and apoptosis. Consequently, selegiline may be advantageous in the long-term treatment of PD.
What this study adds
Evidence grade: Low
This is a narrative review. This review of Parkinson's disease describes evidence of oxidative stress, including altered brain iron, impaired mitochondrial function, and changes in antioxidant systems such as superoxide dismutase and reduced glutathione. A loss of glutathione is associated with incidental Lewy body disease and may be the earliest biochemical marker of nigral cell loss, though glutathione depletion alone may not damage nigral neurons but may increase susceptibility to later toxic or free radical exposure.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Jenner, P., & Olanow, C. W. (1996). Oxidative stress and the pathogenesis of Parkinson's disease. Neurology. https://doi.org/10.1212/wnl.47.6_suppl_3.161s
Vancouver
Jenner P, Olanow CW. Oxidative stress and the pathogenesis of Parkinson's disease. Neurology. 1996. doi:10.1212/wnl.47.6_suppl_3.161s. PMID: 8959985.
BibTeX
@article{jenner1996-8959985,
author = {Jenner, P. and Olanow, C. W.},
title = {{Oxidative stress and the pathogenesis of Parkinson's disease}},
journal = {Neurology},
year = {1996},
doi = {10.1212/wnl.47.6_suppl_3.161s},
pmid = {8959985},
url = {https://doi.org/10.1212/wnl.47.6_suppl_3.161s}
}
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
- A loss of GSH is associated with incidental Lewy body disease and may represent the earliest biochemical marker of nigral cell loss.
- GSH depletion alone may not result in damage to nigral neurons but may increase susceptibility to subsequent toxic or free radical exposure.
Why it matters
This review of Parkinson's disease describes evidence of oxidative stress, including altered brain iron, impaired mitochondrial function, and changes in antioxidant systems such as superoxide dismutase and reduced glutathione. A loss of glutathione is associated with incidental Lewy body disease and may be the earliest biochemical marker of nigral cell loss, though glutathione depletion alone may not damage nigral neurons but may increase susceptibility to later toxic or free radical exposure.
Study details
- Evidence strengthLow
How this study scored 50/100
Published in a leading specialty 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 | 9 / 10 | Tier 2 — leading specialty journal (Neurology) |
| Journal's citation record | 4 / 4 | Neurology: journal h-index 525 (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 | 1996 — older than 20 years, still counted |
| 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 976 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 30.5 citations a year over 32 year(s) since 1996 |
| Impact for its field and year | 5 / 6 | Cited 29.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 2 / 4 | Cited 36 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author C. Warren Olanow: h-index 117 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | King's College London: institution h-index 1,348 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 8959985) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 50 / 100 | — |
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