This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

45/100

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Risk genes beyond APOE

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer disease is the most common cause of dementia and represents a major public health problem. The neuropathologic findings of amyloid-beta plaques and tau containing neurofibrillary tangles represent important molecular clues to the underlying pathogenesis. Genetic factors are well recognized, but complicated.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Bird, T. D. (2008). Genetic aspects of Alzheimer disease. Genetics in medicine : official journal of the American College of Medical Genetics. https://doi.org/10.1097/gim.0b013e31816b64dc

Vancouver

Bird TD. Genetic aspects of Alzheimer disease. Genetics in medicine : official journal of the American College of Medical Genetics. 2008. doi:10.1097/gim.0b013e31816b64dc. PMID: 18414205.

BibTeX

@article{bird2008-18414205,
  author  = {Bird, T. D.},
  title   = {{Genetic aspects of Alzheimer disease}},
  journal = {Genetics in medicine : official journal of the American College of Medical Genetics},
  year    = {2008},
  doi     = {10.1097/gim.0b013e31816b64dc},
  pmid    = {18414205},
  url     = {https://doi.org/10.1097/gim.0b013e31816b64dc}
}

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.

Key findings

The neuropathologic findings of amyloid-beta plaques and tau containing neurofibrillary tangles represent important molecular clues to the underlying pathogenesis.
Genetic factors are well recognized, but complicated.
Three rare forms of autosomal-dominant early-onset familial Alzheimer disease have been identified and are associated with mutations in amyloid precursor protein, presenilin 1, and presenilin 2 genes.
The more common late-onset form of Alzheimer disease is assumed to be polygenic/multifactorial.

Why it matters

This review describes the genetics of Alzheimer's disease, including rare autosomal-dominant early-onset forms linked to mutations in amyloid precursor protein, presenilin 1 and presenilin 2, and the more common late-onset form assumed to be polygenic. It explains genetic factors but does not present a treatment, cure or prevention.

New to this subject? Start with our plain-English guide: Genetics →

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 senior author's track 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 (Genetics in medicine : official journal of the American College of Medical Genetics)
Journal's citation record	2 / 4	Genetics in Medicine: journal h-index 204 (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	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	5 / 7	Cited 291 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	14.6 citations a year over 20 year(s) since 2008
Impact for its field and year	4 / 6	Cited 17.1× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 8 other studies in this library
Still being cited	2 / 4	Cited 42 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	3 / 3	University of Washington: institution h-index 3,540 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 18414205)
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 →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Studies in the library that share something with this one. The line above each title says what.

Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here.

Later studies that cite this one

8 studies in the alzhub library list this one in their references.

Related studies in Risk genes beyond APOE

Also in Risk genes beyond APOE

105 studies in the library are filed under Risk genes beyond APOE with no topic tag they share with another; these are this study's neighbours in a fixed tour of them. The Risk genes beyond APOE hub.

Similar studies

More on Risk genes beyond APOE

See all studies in Risk genes beyond APOE →