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The aging brain
Yankner BA, Lu T, Loerch P.. Annual review of pathology, 2008-01-01
Topic: Risk, prevention and care in population studies
Aging is accompanied by cognitive decline in a major segment of the population and is the primary risk factor for Alzheimer's disease and other prevalent neurodegenerative disorders. Despite this central role in disease pathogenesis and morbidity, the aging of the brain has not been well understood at a molecular level. This review seeks to integrate what is known about age-related cognitive and neuroanatomical changes with recent advances in understanding basic molecular mechanisms that underlie aging. An important issue is how normal brain aging transitions to pathological aging, giving rise to neurodegenerative disorders. Toxic protein aggregates have been identified as potential contributory factors, including amyloid beta-protein in Alzheimer's disease, tau in frontotemporal dementia, and alpha-synuclein in Parkinson's disease. However, current models of pathogenesis do not explain the origin of the common sporadic forms of these diseases or address the critical nexus between aging and disease. This review discusses potential approaches to unifying the systems biology of the aging brain with the pathogenesis of neurodegeneration.
Key findings
- This review seeks to integrate what is known about age-related cognitive and neuroanatomical changes with recent advances in understanding basic molecular mechanisms that underlie aging.
- An important issue is how normal brain aging transitions to pathological aging, giving rise to neurodegenerative disorders.
- Toxic protein aggregates have been identified as potential contributory factors, including amyloid beta-protein in Alzheimer's disease, tau in frontotemporal dementia, and alpha-synuclein in Parkinson's disease.
- However, current models of pathogenesis do not explain the origin of the common sporadic forms of these diseases or address the critical nexus between aging and disease.
- This review discusses potential approaches to unifying the systems biology of the aging brain with the pathogenesis of neurodegeneration.
Why it matters
This review discusses how normal brain aging transitions to pathological aging and notes that toxic protein aggregates including amyloid beta-protein are potential contributory factors in Alzheimer's disease. It is a discussion of mechanisms and does not report a tested treatment, cure, or prevention.
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Study details
- Evidence strengthLow
How this study scored 45/100
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. We have no data on journal's citation record, so that was left out: it earned 43 of the 96 points we could judge it on, which is 45 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Annual review of pathology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2008 — 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 | 6 / 7 | Cited 676 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 33.8 citations a year over 20 year(s) since 2008 |
| Impact for its field and year | 3 / 6 | Cited 3.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 3 / 4 | Cited 73 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Patrick Loerch: h-index 10 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre 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 18039130) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 43 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 43 of the 96 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Yankner, B. A., Lu, T., & Loerch, P. (2008). The aging brain. Annual review of pathology. https://doi.org/10.1146/annurev.pathmechdis.2.010506.092044
Vancouver
Yankner BA, Lu T, Loerch P. The aging brain. Annual review of pathology. 2008. doi:10.1146/annurev.pathmechdis.2.010506.092044. PMID: 18039130.
BibTeX
@article{yankner2008-18039130,
author = {Yankner, B. A. and Lu, T. and Loerch, P.},
title = {{The aging brain}},
journal = {Annual review of pathology},
year = {2008},
doi = {10.1146/annurev.pathmechdis.2.010506.092044},
pmid = {18039130},
url = {https://doi.org/10.1146/annurev.pathmechdis.2.010506.092044}
}
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6 studies in the alzhub library list this one in their references.