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Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms
von Bernhardi R, Eugenín J.. Antioxidants & redox signaling, 2012-02-07
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Alzheimer's disease (AD) is the most common cause of dementia and a progressive neurodegeneration that appears to result from multiple pathogenic mechanisms (including protein misfolding/aggregation, involved in both amyloid β-dependent senile plaques and tau-dependent neurofibrillary tangles), metabolic and mitochondrial dysfunction, excitoxicity, calcium handling impairment, glial cell dysfunction, neuroinflammation, and oxidative stress. Oxidative stress, which could be secondary to several of the other pathophysiological mechanisms, appears to be a major determinant of the pathogenesis and progression of AD. The identification of oxidized proteins common for mild cognitive impairment and AD suggests that key oxidation pathways are triggered early and are involved in the initial progression of the neurodegenerative process. Abundant data support that oxidative stress, also considered as a main factor for aging, the major risk factor for AD, can be a common key element capable of articulating the divergent nature of the proposed pathogenic factors. Pathogenic mechanisms influence each other at different levels. Evidence suggests that it will be difficult to define a single-target therapy resulting in the arrest of progression or the improvement of AD deterioration. Since oxidative stress is present from early stages of disease, it appears as one of the main targets to be included in a clinical trial. Exploring the articulation of AD pathogenic mechanisms by oxidative stress will provide clues for better understanding the pathogenesis and progression of this dementing disorder and for the development of effective therapies to treat this disease.
What this study adds
Evidence grade: Low
This is a narrative review. This review argues that oxidative stress appears to be a major determinant of Alzheimer's disease and is present from early stages, with oxidized proteins found in both mild cognitive impairment and Alzheimer's disease. It concludes that a single-target therapy will likely be difficult to achieve, so oxidative stress is proposed as one of the main targets to investigate.
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
von Bernhardi, R., & Eugenín, J. (2012). Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms. Antioxidants & redox signaling. https://doi.org/10.1089/ars.2011.4082
Vancouver
von Bernhardi R, Eugenín J. Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms. Antioxidants & redox signaling. 2012. doi:10.1089/ars.2011.4082. PMID: 22122400.
BibTeX
@article{vonbernhardi2012-22122400,
author = {von Bernhardi, R. and Eugenín, J.},
title = {{Alzheimer's disease: redox dysregulation as a common denominator for diverse pathogenic mechanisms}},
journal = {Antioxidants \& redox signaling},
year = {2012},
doi = {10.1089/ars.2011.4082},
pmid = {22122400},
url = {https://doi.org/10.1089/ars.2011.4082}
}
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
- Alzheimer's disease (AD) is the most common cause of dementia and a progressive neurodegeneration that appears to result from multiple pathogenic mechanisms (including protein misfolding/aggregation, involved in both amyloid β-dependent senile plaques and tau-dependent neurofibrillary tangles), metabolic and mitochondrial dysfunction, excitoxicity, calcium handling impairment, glial cell dysfunction, neuroinflammation, and oxidative stress.
- The identification of oxidized proteins common for mild cognitive impairment and AD suggests that key oxidation pathways are triggered early and are involved in the initial progression of the neurodegenerative process.
- Evidence suggests that it will be difficult to define a single-target therapy resulting in the arrest of progression or the improvement of AD deterioration.
Why it matters
This review argues that oxidative stress appears to be a major determinant of Alzheimer's disease and is present from early stages, with oxidized proteins found in both mild cognitive impairment and Alzheimer's disease. It concludes that a single-target therapy will likely be difficult to achieve, so oxidative stress is proposed as one of the main targets to investigate.
Study details
- Evidence strengthLow
How this study scored 43/100
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 (Antioxidants & redox signaling) |
| Journal's citation record | 3 / 4 | Antioxidants and Redox Signaling: journal h-index 274 (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 | 2012 — 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 | 5 / 7 | Cited 191 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.9 citations a year over 16 year(s) since 2012 |
| Impact for its field and year | 4 / 6 | Cited 8.9× 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 | 2 / 4 | Cited 27 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jaime L. Eugenín: h-index 21 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | Pontificia Universidad Católica de Chile: institution h-index 508 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22122400) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 43 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1089/ars.2011.4082
- PubMed: 22122400
- Original source →
- Free full text: LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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