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The seminal role of beta-amyloid in the pathogenesis of Alzheimer disease
Joachim CL, Selkoe DJ.. Alzheimer disease and associated disorders, 1992-01-01
Topic: Amyloid, tau and blood-test diagnosis
New molecular information about Alzheimer disease (AD) is appearing at an unprecedented rate. Much interest centers on the beta A4 amyloid protein, which is progressively deposited in senile plaques and blood vessels in AD brain tissue. The discovery that some kindreds with familial AD have a mutation in the gene coding for the beta A4 amyloid precursor protein (APP) suggests that this mutation alone may be sufficient to cause the full spectrum of clinical and pathological changes that characterize AD.
Key findings
- Much interest centers on the beta A4 amyloid protein, which is progressively deposited in senile plaques and blood vessels in AD brain tissue.
- The discovery that some kindreds with familial AD have a mutation in the gene coding for the beta A4 amyloid precursor protein (APP) suggests that this mutation alone may be sufficient to cause the full spectrum of clinical and pathological changes that characterize AD.
- Although APP point mutations may turn out to be relatively rare causes of AD, the idea that accelerated beta A4 deposition is an early and critical event in many patients continues to gain support from studies in humans, animals, and cultured cells.
- Identification of the biochemical steps leading to production of the beta A4 peptide from APP is now a critical issue.
Why it matters
This review argues that beta-amyloid plays a central role in Alzheimer's disease, noting that a mutation in the amyloid precursor protein gene in some families may be enough to cause the full disease. It is a discussion of disease causation and reports no treatment, cure or prevention.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 41/100
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 (Alzheimer disease and associated disorders) |
| Journal's citation record | 1 / 4 | Alzheimer Disease & Associated Disorders: journal h-index 131 (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 | 1992 — 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 | 5 / 7 | Cited 182 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.1 citations a year over 36 year(s) since 1992 |
| Impact for its field and year | 4 / 6 | Cited 11.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 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 | 4 / 4 | Last-listed author Dennis J. Selkoe: h-index 174 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Oxford: institution h-index 2,205 (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 1605946) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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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
Joachim, C. L., & Selkoe, D. J. (1992). The seminal role of beta-amyloid in the pathogenesis of Alzheimer disease. Alzheimer disease and associated disorders. https://doi.org/10.1097/00002093-199205000-00003
Vancouver
Joachim CL, Selkoe DJ. The seminal role of beta-amyloid in the pathogenesis of Alzheimer disease. Alzheimer disease and associated disorders. 1992. doi:10.1097/00002093-199205000-00003. PMID: 1605946.
BibTeX
@article{joachim1992-1605946,
author = {Joachim, C. L. and Selkoe, D. J.},
title = {{The seminal role of beta-amyloid in the pathogenesis of Alzheimer disease}},
journal = {Alzheimer disease and associated disorders},
year = {1992},
doi = {10.1097/00002093-199205000-00003},
pmid = {1605946},
url = {https://doi.org/10.1097/00002093-199205000-00003}
}
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