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Oxidative stress and the pathogenesis of neurodegenerative disorders
Reynolds A, Laurie C, Mosley RL, Gendelman HE.. International review of neurobiology, 2007-01-01
Topic: Brain proteins, microglia and lab models
Microglia-derived inflammatory neurotoxins play a principal role in the pathogenesis of neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and HIV-associated dementia; chief among these is reactive oxygen species. The detrimental effects of oxidative stress in the brain and nervous system are primarily a result of the diminished capacity of the central nervous system to prevent ongoing oxidative damage. A spectrum of environmental cues, mitochondrial dysfunction, accumulation of aberrant misfolded proteins, inflammation, and defects in protein clearance are known to evolve and form as a result of disease progression. These factors likely affect glial function serving to accelerate the tempo of disease. Understanding the relationships between disease progression, free radical formation, neuroinflammation, and neurotoxicity is critical to elucidating disease mechanisms and the development of therapeutic modalities to combat disease processes. In an era where populations continue to age, the prevalence and incidence of age-related neurodegenerative diseases are on the rise; therefore, the need for novel therapeutic strategies that attenuate neuroinflammation and protect neurons against oxidative stress is ever more immediate.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Reynolds, A., Laurie, C., Mosley, R. L., & Gendelman, H. E. (2007). Oxidative stress and the pathogenesis of neurodegenerative disorders. International review of neurobiology. https://doi.org/10.1016/s0074-7742(07)82016-2
Vancouver
Reynolds A, Laurie C, Mosley RL, Gendelman HE. Oxidative stress and the pathogenesis of neurodegenerative disorders. International review of neurobiology. 2007. doi:10.1016/s0074-7742(07)82016-2. PMID: 17678968.
BibTeX
@article{reynolds2007-17678968,
author = {Reynolds, A. and Laurie, C. and Mosley, R. L. and Gendelman, H. E.},
title = {{Oxidative stress and the pathogenesis of neurodegenerative disorders}},
journal = {International review of neurobiology},
year = {2007},
doi = {10.1016/s0074-7742(07)82016-2},
pmid = {17678968},
url = {https://doi.org/10.1016/s0074-7742(07)82016-2}
}
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Key findings
- The detrimental effects of oxidative stress in the brain and nervous system are primarily a result of the diminished capacity of the central nervous system to prevent ongoing oxidative damage.
- A spectrum of environmental cues, mitochondrial dysfunction, accumulation of aberrant misfolded proteins, inflammation, and defects in protein clearance are known to evolve and form as a result of disease progression.
Why it matters
This review describes how oxidative stress and inflammation from microglia are involved in the pathogenesis of neurodegenerative disorders including Alzheimer's disease. It discusses possible therapeutic directions but reports no tested treatment or cure.
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Study details
- Evidence strengthLow
How this study scored 48/100
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. We have no data on journal's citation record, so that was left out: it earned 46 of the 96 points we could judge it on, which is 48 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (International review of neurobiology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2007 — 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 434 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 20.7 citations a year over 21 year(s) since 2007 |
| Impact for its field and year | 6 / 6 | Cited 59.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 3 other studies in this library |
| Still being cited | 3 / 4 | Cited 50 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Howard Eliot Gendelman: h-index 110 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | University of Nebraska Medical Center: institution h-index 666 (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 17678968) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 46 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 46 of the 96 points we could judge it on is 48 out of 100. |
| Total | 48 / 100 | — |
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