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Evidence of increased oxidative damage in subjects with mild cognitive impairment
Keller JN, Schmitt FA, Scheff SW, Ding Q, Chen Q, Butterfield DA, Markesbery WR.. Neurology, 2005-04-01
Topic: Risk, prevention and care in population studies
Objective To determine if increased levels of oxidative damage are present in the brains of persons with mild cognitive impairment (MCI), a condition that often precedes Alzheimer disease (AD). Methods The authors assessed the amount of protein carbonyls, thiobarbituric acid-reactive substances (TBARS), and malondialdehyde in the superior and middle temporal gyri (SMTG) and cerebellum of short postmortem interval and longitudinally evaluated normal subjects and those with MCI and early AD. Results Elevated levels of protein carbonyls (approximately 25%), malondialdehyde (approximately 60%), and TBARS (approximately 210%) were observed in the SMTG of individuals with MCI and early AD vs normal control subjects. The elevation in TBARS was associated with the numbers of neuritic but not diffuse plaques. Levels of protein carbonyls increased as delayed verbal memory performance declined. Conclusion Oxidative damage occurs in the brain of subjects with mild cognitive impairment, suggesting that oxidative damage may be one of the earliest events in the onset and progression of Alzheimer disease.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Keller, J. N., Schmitt, F. A., Scheff, S. W., Ding, Q., Chen, Q., Butterfield, D. A., et al. (2005). Evidence of increased oxidative damage in subjects with mild cognitive impairment. Neurology. https://doi.org/10.1212/01.wnl.0000156156.13641.ba
Vancouver
Keller JN, Schmitt FA, Scheff SW, Ding Q, Chen Q, Butterfield DA, et al. Evidence of increased oxidative damage in subjects with mild cognitive impairment. Neurology. 2005. doi:10.1212/01.wnl.0000156156.13641.ba. PMID: 15824339.
BibTeX
@article{keller2005-15824339,
author = {Keller, J. N. and Schmitt, F. A. and Scheff, S. W. and Ding, Q. and Chen, Q. and Butterfield, D. A. and Markesbery, W. R.},
title = {{Evidence of increased oxidative damage in subjects with mild cognitive impairment}},
journal = {Neurology},
year = {2005},
doi = {10.1212/01.wnl.0000156156.13641.ba},
pmid = {15824339},
url = {https://doi.org/10.1212/01.wnl.0000156156.13641.ba}
}
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 names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Results Elevated levels of protein carbonyls (approximately 25%), malondialdehyde (approximately 60%), and TBARS (approximately 210%) were observed in the SMTG of individuals with MCI and early AD vs normal control subjects.
- The elevation in TBARS was associated with the numbers of neuritic but not diffuse plaques.
- Conclusion Oxidative damage occurs in the brain of subjects with mild cognitive impairment, suggesting that oxidative damage may be one of the earliest events in the onset and progression of Alzheimer disease.
Why it matters
In brain tissue examined soon after death, people with mild cognitive impairment or early Alzheimer's (reported as one combined group) had higher levels of three oxidative-damage markers in a temporal-lobe region than cognitively normal people: about 25% more protein carbonyls, 60% more malondialdehyde and 210% more TBARS. Higher TBARS went with more neuritic plaques, and higher protein carbonyls went with worse delayed verbal memory. The authors suggest oxidative damage "may be one of the earliest events" in Alzheimer's, but this is a single after-death measurement that shows an association, not a cause, and it tested no treatment.
Study details
- Evidence strengthLow
How this study scored 52/100
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 | 2005 — 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 540 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 23.5 citations a year over 23 year(s) since 2005 |
| Impact for its field and year | 4 / 6 | Cited 19.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 38 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 | 4 / 4 | Last-listed author William R. Markesbery: h-index 124 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Kentucky: institution h-index 824 (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 15824339) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 52 / 100 | — |
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