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46/100

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Genetics

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

Objective To evaluate the association of risk and age at onset (AAO) of Alzheimer disease (AD) with single-nucleotide polymorphisms (SNPs) in the chromosome 19 region including apolipoprotein E (APOE) and a repeat-length polymorphism in TOMM40 (poly-T, rs10524523). Design Conditional logistic regression models and survival analysis. Setting Fifteen genome-wide association study data sets assembled by the Alzheimer's Disease Genetics Consortium. Participants Eleven thousand eight hundred forty AD cases and 10 931 cognitively normal elderly controls. Main outcome measures Association of AD risk and AAO with genotyped and imputed SNPs located in an 800-Mb region including APOE in the entire Alzheimer's Disease Genetics Consortium data set and with the TOMM40 poly-T marker genotyped in a subset of 1256 cases and 1605 controls. Results In models adjusting for APOE ε4, no SNPs in the entire region were significantly associated with AAO at P.001. Rs10524523 was not significantly associated with AD or AAO in models adjusting for APOE genotype or within the subset of ε3/ε3 subjects. Conclusions APOE alleles ε2, ε3, and ε4 account for essentially all the inherited risk of AD associated with this region. Other variants including a poly-T track in TOMM40 are not independent risk or AAO loci.

What this study adds

Evidence grade: Low

This large genetic analysis found that APOE alleles ε2, ε3, and ε4 account for essentially all the inherited risk of Alzheimer disease associated with this chromosome region. Other variants tested, including a poly-T track in TOMM40, were not independent risk or age-at-onset loci.

Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.

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

APA 7th

Jun, G., Vardarajan, B. N., Buros, J., Yu, C. E., Hawk, M. V., Dombroski, B. A., et al. (2012). Comprehensive search for Alzheimer disease susceptibility loci in the APOE region. Archives of neurology. https://doi.org/10.1001/archneurol.2012.2052

Vancouver

Jun G, Vardarajan BN, Buros J, Yu CE, Hawk MV, Dombroski BA, et al. Comprehensive search for Alzheimer disease susceptibility loci in the APOE region. Archives of neurology. 2012. doi:10.1001/archneurol.2012.2052. PMID: 22869155.

BibTeX

@article{jun2012-22869155,
  author  = {Jun, G. and Vardarajan, B. N. and Buros, J. and Yu, C. E. and Hawk, M. V. and Dombroski, B. A. and Crane, P. K. and Larson, E. B. and others},
  title   = {{Comprehensive search for Alzheimer disease susceptibility loci in the APOE region}},
  journal = {Archives of neurology},
  year    = {2012},
  doi     = {10.1001/archneurol.2012.2052},
  pmid    = {22869155},
  url     = {https://doi.org/10.1001/archneurol.2012.2052}
}

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How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Results In models adjusting for APOE ε4, no SNPs in the entire region were significantly associated with AAO at P.001.
Rs10524523 was not significantly associated with AD or AAO in models adjusting for APOE genotype or within the subset of ε3/ε3 subjects.
Conclusions APOE alleles ε2, ε3, and ε4 account for essentially all the inherited risk of AD associated with this region.

Why it matters

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Study details

Evidence strengthLow

How this study scored 46/100

Published in a peer-reviewed 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	7 / 10	Tier 3 — peer-reviewed journal (Archives of neurology)
Journal's citation record	3 / 4	Archives of Neurology: journal h-index 353 (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	2012 — 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	5 / 7	Cited 106 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	6.6 citations a year over 16 year(s) since 2012
Impact for its field and year	3 / 6	Cited 7.2× 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	1 / 4	Cited 5 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Lindsay A. Farrer: h-index 119 (OpenAlex, whole career)
Institution's track record	3 / 3	University of Washington: institution h-index 3,540 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 8 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 22869155)
Free to read	0 / 2	Behind a paywall — scores zero
Total	46 / 100	—

What each of these 20 components measures, and what this score is not →

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