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Alzheimer's disease is not "brain aging": neuropathological, genetic, and epidemiological human studies
Nelson PT, Head E, Schmitt FA, Davis PR, Neltner JH, Jicha GA, Abner EL, Smith CD et al.. Acta neuropathologica, 2011-04-24
Topic: Amyloid, tau and blood-test diagnosis
Human studies are reviewed concerning whether "aging"-related mechanisms contribute to Alzheimer's disease (AD) pathogenesis. AD is defined by specific neuropathology: neuritic amyloid plaques and neocortical neurofibrillary tangles. AD pathology is driven by genetic factors related not to aging per se, but instead to the amyloid precursor protein (APP). In contrast to genes involved in APP-related mechanisms, there is no firm connection between genes implicated in human "accelerated aging" diseases (progerias) and AD. The epidemiology of AD in advanced age is highly relevant but deceptively challenging to address given the low autopsy rates in most countries. In extreme old age, brain diseases other than AD approximate AD prevalence while the impact of AD pathology appears to peak by age 95 and decline thereafter. Many distinct brain diseases other than AD afflict older human brains and contribute to cognitive impairment. Additional prevalent pathologies include cerebrovascular disease and hippocampal sclerosis, both high-morbidity brain diseases that appear to peak in incidence later than AD chronologically. Because of these common brain diseases of extreme old age, the epidemiology differs between clinical "dementia" and the subset of dementia cases with AD pathology. Additional aging-associated mechanisms for cognitive decline such as diabetes and synapse loss have been linked to AD and these hypotheses are discussed. Criteria are proposed to define an "aging-linked" disease, and AD fails all of these criteria. In conclusion, it may be most fruitful to focus attention on specific pathways involved in AD rather than attributing it to an inevitable consequence of aging.
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APA 7th
Nelson, P. T., Head, E., Schmitt, F. A., Davis, P. R., Neltner, J. H., Jicha, G. A., et al. (2011). Alzheimer's disease is not "brain aging": neuropathological, genetic, and epidemiological human studies. Acta neuropathologica. https://doi.org/10.1007/s00401-011-0826-y
Vancouver
Nelson PT, Head E, Schmitt FA, Davis PR, Neltner JH, Jicha GA, et al. Alzheimer's disease is not "brain aging": neuropathological, genetic, and epidemiological human studies. Acta neuropathologica. 2011. doi:10.1007/s00401-011-0826-y. PMID: 21516511.
BibTeX
@article{nelson2011-21516511,
author = {Nelson, P. T. and Head, E. and Schmitt, F. A. and Davis, P. R. and Neltner, J. H. and Jicha, G. A. and Abner, E. L. and Smith, C. D. and others},
title = {{Alzheimer's disease is not "brain aging": neuropathological, genetic, and epidemiological human studies}},
journal = {Acta neuropathologica},
year = {2011},
doi = {10.1007/s00401-011-0826-y},
pmid = {21516511},
url = {https://doi.org/10.1007/s00401-011-0826-y}
}
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Key findings
- In conclusion, it may be most fruitful to focus attention on specific pathways involved in AD rather than attributing it to an inevitable consequence of aging.
Why it matters
This review argues that Alzheimer's disease is defined by specific neuropathology driven by genetic factors related to amyloid precursor protein, not by aging itself. It concludes it may be most fruitful to focus on specific pathways involved in Alzheimer's disease rather than attributing it to an inevitable consequence of aging.
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Study details
- Evidence strengthLow
How this study scored 51/100
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 (Acta neuropathologica) |
| Journal's citation record | 3 / 4 | Acta Neuropathologica: journal h-index 287 (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 | 2011 — 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 366 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 21.5 citations a year over 17 year(s) since 2011 |
| Impact for its field and year | 4 / 6 | Cited 13.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 33 other studies in this library |
| Still being cited | 3 / 4 | Cited 75 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Stephen W. Scheff: h-index 86 (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 21516511) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
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