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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 60 out of 100. Genetics

Topic: Amyloid, tau and blood-test diagnosis

Objective To determine whether APOE epsilon 4 predicts rate of cognitive change in incident and prevalent Alzheimer disease (AD). Methods Individuals were recruited from two longitudinal cohort studies-the Washington Heights and Inwood Columbia Aging Project (WHICAP; population-based) and the Predictors Study (clinic-based)--and were followed for an average of 4 years. Three samples of participants diagnosed with AD, with diverse demographic characteristics and baseline cognitive functioning, were studied: 1) 199 (48%) of the incident WHICAP cases; 2) 215 (54%) of the prevalent WHICAP cases; and 3) 156 (71%) of the individuals diagnosed with AD in the Predictors Study. Generalized estimating equations were used to test whether rate of cognitive change, measured using a composite cognitive score in WHICAP and the Mini-Mental State Examination in Predictors, varied as a function of epsilon 4 status in each sample. Results The presence of at least one epsilon 4 allele was associated with faster cognitive decline in the incident population-based AD group (p = 0.01). Parallel results were produced for the two prevalent dementia samples only when adjusting for disease severity or excluding the most impaired participants from the analyses. Conclusion APOE epsilon 4 may influence rate of cognitive decline most significantly in the earliest stages of Alzheimer disease.

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

APA 7th

Cosentino, S., Scarmeas, N., Helzner, E., Glymour, M. M., Brandt, J., Albert, M., et al. (2008). APOE epsilon 4 allele predicts faster cognitive decline in mild Alzheimer disease. Neurology. https://doi.org/10.1212/01.wnl.0000304038.37421.cc

Vancouver

Cosentino S, Scarmeas N, Helzner E, Glymour MM, Brandt J, Albert M, et al. APOE epsilon 4 allele predicts faster cognitive decline in mild Alzheimer disease. Neurology. 2008. doi:10.1212/01.wnl.0000304038.37421.cc. PMID: 18401023.

BibTeX

@article{cosentino2008-18401023,
  author  = {Cosentino, S. and Scarmeas, N. and Helzner, E. and Glymour, M. M. and Brandt, J. and Albert, M. and Blacker, D. and Stern, Y.},
  title   = {{APOE epsilon 4 allele predicts faster cognitive decline in mild Alzheimer disease}},
  journal = {Neurology},
  year    = {2008},
  doi     = {10.1212/01.wnl.0000304038.37421.cc},
  pmid    = {18401023},
  url     = {https://doi.org/10.1212/01.wnl.0000304038.37421.cc}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

Key findings

Why it matters

In population-based and clinic-based samples, the presence of at least one APOE epsilon4 allele was associated with faster cognitive decline in the incident population-based Alzheimer disease group, with parallel results in prevalent samples only after adjustment or exclusions. The findings suggest APOE epsilon4 may influence rate of decline most in the earliest stages, but no treatment was tested.

Study details

How this study scored 60/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 4 of 4; Study design 7 of 12; Strength of evidence 3 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 0 of 3; Randomised / blinded 0 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 3 of 6; Still being cited 2 of 4; Senior author's track record 4 of 4; Institution's track record 2 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 60 of 100.60 of 100 points earned40 not earned

Published in a leading specialty journal, and it is a cohort study following people over time. Scored zero for sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (Neurology)
Journal's citation record 4 / 4 Neurology: journal h-index 525 (OpenAlex, 2026-10-29)
Study design 7 / 12 A cohort study following people over time
Strength of evidence 3 / 5 Rated “moderate” 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 215 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 10.8 citations a year over 20 year(s) since 2008
Impact for its field and year 4 / 6 Cited 11.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 15 other studies in this library
Still being cited 2 / 4 Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Yaakov Stern: h-index 162 (OpenAlex, whole career)
Institution's track record 2 / 3 Columbia University: institution h-index 1,824 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 18401023)
Free to read 0 / 2 Behind a paywall — scores zero
Total 60 / 100 —

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

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