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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.

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Genetics

Topic: Amyloid, tau and blood-test diagnosis

Risk information for Alzheimer disease (AD) may be communicated through susceptibility gene disclosure, even though this is not currently in clinical use. The REVEAL Study is the first randomized clinical trial of risk assessment for AD with apolipoprotein E (APOE) genotype and numerical risk estimate disclosure. We examined whether APOE genotype and numerical risk disclosure to asymptomatic individuals at high risk for AD alters health behaviors. One hundred sixty-two participants were randomized to either intervention (APOE disclosure) or control (no genotype disclosure) groups. Subjects in both groups received numerical lifetime risk estimates of future AD development based on sex and family history of AD. The intervention group received their APOE genotype. Subjects were informed that no proven preventive measures for AD existed and given an information sheet on preventative therapies under investigation. Participants who learned they were epsilon 4 positive were significantly more likely than epsilon 4 negative participants to report AD-specific health behavior change 1 year after disclosure (adjusted odds ratio: 2.73; 95% confidence interval: 1.14, 6.54; P=0.02). Post hoc analyses revealed similar significant associations between numerical lifetime risk estimates and self-report of AD-specific health behavior change. Despite lack of preventive measures for AD, knowledge of APOE genotype, numerical lifetime risk, or both, influences health behavior.

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

APA 7th

Chao, S., Roberts, J. S., Marteau, T. M., Silliman, R., Cupples, L. A., & Green, R. C. (2008). Health behavior changes after genetic risk assessment for Alzheimer disease: The REVEAL Study. Alzheimer disease and associated disorders. https://doi.org/10.1097/wad.0b013e31815a9dcc

Vancouver

Chao S, Roberts JS, Marteau TM, Silliman R, Cupples LA, Green RC. Health behavior changes after genetic risk assessment for Alzheimer disease: The REVEAL Study. Alzheimer disease and associated disorders. 2008. doi:10.1097/wad.0b013e31815a9dcc. PMID: 18317253.

BibTeX

@article{chao2008-18317253,
  author  = {Chao, S. and Roberts, J. S. and Marteau, T. M. and Silliman, R. and Cupples, L. A. and Green, R. C.},
  title   = {{Health behavior changes after genetic risk assessment for Alzheimer disease: The REVEAL Study}},
  journal = {Alzheimer disease and associated disorders},
  year    = {2008},
  doi     = {10.1097/wad.0b013e31815a9dcc},
  pmid    = {18317253},
  url     = {https://doi.org/10.1097/wad.0b013e31815a9dcc}
}

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

Why it matters

In this randomized trial, people who learned they were APOE epsilon4 positive were more likely to report Alzheimer-specific health behavior changes one year later than those who learned they were epsilon4 negative. Participants were told no proven preventive measures for Alzheimer disease existed, so the study concerns behavior after risk disclosure, not a treatment or cure.

Study details

How this study scored 63/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 1 of 4; Study design 11 of 12; Strength of evidence 5 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 3 of 3; Randomised / blinded 1 of 2; Times cited 5 of 7; Citations per year 3 of 5; Impact for its field and year 4 of 6; Cited by studies here 2 of 6; Still being cited 2 of 4; Senior author's track record 2 of 4; Institution's track record 2 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 63 of 100.63 of 100 points earned37 not earned

Published in a peer-reviewed journal, and it is a randomised controlled trial. Scored zero for sample size and effect reported because the record does not state it.

ComponentPointsWhy
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 11 / 12 A randomised controlled trial (from PubMed type “Randomized Controlled Trial”)
Strength of evidence 5 / 5 Rated “high” 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 3 / 3 Studied in people (pubmed indexes it as a clinical or observational study)
Randomised / blinded 1 / 2 Randomised (as stated in the record)
Times cited 5 / 7 Cited 243 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 12.2 citations a year over 20 year(s) since 2008
Impact for its field and year 4 / 6 Cited 9.6× 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 2 / 4 Cited 32 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 2 / 4 Last-listed author Robert C. Green: h-index 32 (OpenAlex, whole career)
Institution's track record 2 / 3 University of Michigan: institution h-index 2,240 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 4 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 18317253)
Free to read 0 / 2 Behind a paywall — scores zero
Total 63 / 100 —

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

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