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Defective DNA base excision repair in brain from individuals with Alzheimer's disease and amnestic mild cognitive impairment
Weissman L, Jo DG, Sørensen MM, de Souza-Pinto NC, Markesbery WR, Mattson MP, Bohr VA.. Nucleic acids research, 2007-08-17
Topic: Amyloid, tau and blood-test diagnosis
Oxidative stress is thought to play a role in the pathogenesis of Alzheimer's disease (AD) and increased oxidative DNA damage has been observed in brain tissue from AD patients. Base excision repair (BER) is the primary DNA repair pathway for small base modifications such as alkylation, deamination and oxidation. In this study, we have investigated alterations in the BER capacity in brains of AD patients. We employed a set of functional assays to measure BER activities in brain tissue from short post-mortem interval autopsies of 10 sporadic AD patients and 10 age-matched controls. BER activities were also measured in brain samples from 9 amnestic mild cognitive impairment (MCI) subjects. We found significant BER deficiencies in brains of AD patients due to limited DNA base damage processing by DNA glycosylases and reduced DNA synthesis capacity by DNA polymerase beta. The BER impairment was not restricted to damaged brain regions and was also detected in the brains of amnestic MCI patients, where it correlated with the abundance of neurofibrillary tangles. These findings suggest that BER dysfunction is a general feature of AD brains which could occur at the earliest stages of the disease. The results support the hypothesis that defective BER may play an important role in the progression of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Weissman, L., Jo, D. G., Sørensen, M. M., de Souza-Pinto, N. C., Markesbery, W. R., Mattson, M. P., et al. (2007). Defective DNA base excision repair in brain from individuals with Alzheimer's disease and amnestic mild cognitive impairment. Nucleic acids research. https://doi.org/10.1093/nar/gkm605
Vancouver
Weissman L, Jo DG, Sørensen MM, de Souza-Pinto NC, Markesbery WR, Mattson MP, et al. Defective DNA base excision repair in brain from individuals with Alzheimer's disease and amnestic mild cognitive impairment. Nucleic acids research. 2007. doi:10.1093/nar/gkm605. PMID: 17704129.
BibTeX
@article{weissman2007-17704129,
author = {Weissman, L. and Jo, D. G. and Sørensen, M. M. and de Souza-Pinto, N. C. and Markesbery, W. R. and Mattson, M. P. and Bohr, V. A.},
title = {{Defective DNA base excision repair in brain from individuals with Alzheimer's disease and amnestic mild cognitive impairment}},
journal = {Nucleic acids research},
year = {2007},
doi = {10.1093/nar/gkm605},
pmid = {17704129},
url = {https://doi.org/10.1093/nar/gkm605}
}
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
- We found significant BER deficiencies in brains of AD patients due to limited DNA base damage processing by DNA glycosylases and reduced DNA synthesis capacity by DNA polymerase beta.
- These findings suggest that BER dysfunction is a general feature of AD brains which could occur at the earliest stages of the disease.
- The results support the hypothesis that defective BER may play an important role in the progression of AD.
Why it matters
Brain tissue from 10 people with Alzheimer's disease and 9 with amnestic mild cognitive impairment showed reduced DNA base excision repair activity, linked to limited damage processing by DNA glycosylases and reduced DNA synthesis by polymerase beta. The authors suggest this repair defect is a general feature of Alzheimer's brains that may occur early in the disease.
Study details
- Evidence strengthLow
How this study scored 52/100
Published in a peer-reviewed journal. 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 | 7 / 10 | Tier 3 — peer-reviewed journal (Nucleic acids research) |
| Journal's citation record | 4 / 4 | Nucleic Acids Research: journal h-index 869 (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 | 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 299 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 14.2 citations a year over 21 year(s) since 2007 |
| 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 4 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 Vilhelm A. Bohr: h-index 121 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | National Institutes of Health: institution h-index 2,723 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 17704129) |
| Free to read | 2 / 2 | Free to read |
| Total | 52 / 100 | — |
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