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Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease
Davis RE, Miller S, Herrnstadt C, Ghosh SS, Fahy E, Shinobu LA, Galasko D, Thal LJ et al.. Proceedings of the National Academy of Sciences of the United States of America, 1997-04-01
This paper has been retracted. The record we hold marks it as a retracted publication. Check the original source below for the retraction notice before relying on anything it reports.
Topic: Brain proteins, microglia and lab models
Mounting evidence suggests that defects in energy metabolism contribute to the pathogenesis of Alzheimer disease (AD). Cytochrome c oxidase (CO) is kinetically abnormal, and its activity is decreased in brain and peripheral tissue in late-onset AD. CO is encoded by both the mitochondrial and the nuclear genomes.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Davis, R. E., Miller, S., Herrnstadt, C., Ghosh, S. S., Fahy, E., Shinobu, L. A., et al. (1997). Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America. https://doi.org/10.1073/pnas.94.9.4526
Vancouver
Davis RE, Miller S, Herrnstadt C, Ghosh SS, Fahy E, Shinobu LA, et al. Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America. 1997. doi:10.1073/pnas.94.9.4526. PMID: 9114023.
BibTeX
@article{davis1997-9114023,
author = {Davis, R. E. and Miller, S. and Herrnstadt, C. and Ghosh, S. S. and Fahy, E. and Shinobu, L. A. and Galasko, D. and Thal, L. J. and others},
title = {{Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease}},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {1997},
doi = {10.1073/pnas.94.9.4526},
pmid = {9114023},
url = {https://doi.org/10.1073/pnas.94.9.4526}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- Cytochrome c oxidase (CO) is kinetically abnormal, and its activity is decreased in brain and peripheral tissue in late-onset AD.
- CO is encoded by both the mitochondrial and the nuclear genomes.
- Its catalytic centers, however, are encoded exclusively by two mitochondrial genes, CO1 and CO2 (encoding CO subunits I and II, respectively).
- We searched these genes, as well as other mitochondrial genes, for mutations that might alter CO activity and cosegregate with AD.
Why it matters
This study searched mitochondrial genes, including CO1 and CO2, for mutations that might alter cytochrome c oxidase activity and cosegregate with late-onset Alzheimer's disease. It is genetic research into a possible disease mechanism and does not provide a treatment, cure, or prevention.
Study details
- Evidence strengthLow
How this study scored 16/100
Retracted — do not rely on it. It scored 27 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (Proceedings of the National Academy of Sciences of the United States of America) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| 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 | 0 / 10 | Retracted — do not rely on it. PubMed indexes it as a Retracted Publication. |
| How recent | 1 / 5 | 1997 — 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 343 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.1 citations a year over 31 year(s) since 1997 |
| Impact for its field and year | 4 / 6 | Cited 16.9× 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 | 0 / 4 | Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author William Davis Parker: h-index 51 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Massachusetts General Hospital: institution h-index 2,057 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9114023) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 27 / 100 | Capped to 16 because this is not a peer-reviewed article. |
What each of these 20 components measures, and what this score is not →
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