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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 65 out of 100. Genetics

Topic: Amyloid, tau and blood-test diagnosis

Objective To examine whether β-amyloid (Aβ) and APOE ε4 status independently contribute or interact to influence longitudinal cognitive decline in clinically normal older individuals (CN). Methods Data from 490 CNs were aggregated across 3 observational cohort studies (Harvard Aging Brain Study, Alzheimer's Disease Neuroimaging Initiative, and Australian Imaging Biomarkers and Lifestyle Study of Ageing; median age = 75.0 years, 255 female), and the contributions of APOE ε4 and Aβ on longitudinal change over a median of 1.49 years were examined. Cognitive decline was assessed with the Mini-Mental State Examination (MMSE) and Logical Memory (immediate and delayed recall scores). Results High Aβ participants were more likely to be APOE ε4+ than low Aβ participants. CNs who were both high Aβ and APOE ε4+ showed greater decline in Logical Memory immediate recall (p Conclusions Clinically normal individuals who are APOE ε4+ and have high Aβ showed the highest cognitive decline. These results suggest that Aβ and APOE ε4 are not redundant contributors of decline in aging but rather interact to promote decline during the short follow-up period examined in this study. Longer follow-up periods will be essential to fully elucidate the influence of Alzheimer disease risk factors on cognitive decline in aging.

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

APA 7th

Mormino, E. C., Betensky, R. A., Hedden, T., Schultz, A. P., Ward, A., Huijbers, W., et al. (2014). Amyloid and APOE ε4 interact to influence short-term decline in preclinical Alzheimer disease. Neurology. https://doi.org/10.1212/wnl.0000000000000431

Vancouver

Mormino EC, Betensky RA, Hedden T, Schultz AP, Ward A, Huijbers W, et al. Amyloid and APOE ε4 interact to influence short-term decline in preclinical Alzheimer disease. Neurology. 2014. doi:10.1212/wnl.0000000000000431. PMID: 24748674.

BibTeX

@article{mormino2014-24748674,
  author  = {Mormino, E. C. and Betensky, R. A. and Hedden, T. and Schultz, A. P. and Ward, A. and Huijbers, W. and Rentz, D. M. and Johnson, K. A. and others},
  title   = {{Amyloid and APOE ε4 interact to influence short-term decline in preclinical Alzheimer disease}},
  journal = {Neurology},
  year    = {2014},
  doi     = {10.1212/wnl.0000000000000431},
  pmid    = {24748674},
  url     = {https://doi.org/10.1212/wnl.0000000000000431}
}

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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Why it matters

Among clinically normal older adults followed for a median of about 1.5 years, those who had both high amyloid and the APOE epsilon4 allele showed the greatest decline in memory. The authors conclude that amyloid and APOE epsilon4 interact to promote short-term decline, but they note that longer follow-up is needed and no treatment or prevention is tested.

Study details

How this study scored 65/100
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 4 of 5; Impact for its field and year 5 of 6; Cited by studies here 4 of 6; Still being cited 3 of 4; Senior author's track record left out, no data; Institution's track record 3 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. 62 of the 96 points it could be judged on, which is 65 of 100. Total 65 of 100.62 of the 96 points we could judge = 65 of 100

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. We have no data on senior author's track record, so that was left out: it earned 62 of the 96 points we could judge it on, which is 65 out of 100.

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 2014 — 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 295 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 21.1 citations a year over 14 year(s) since 2014
Impact for its field and year 5 / 6 Cited 23.7× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 4 / 6 Cited by 35 other studies in this library
Still being cited 3 / 4 Cited 50 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 Harvard University: institution h-index 3,235 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 4 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 24748674)
Free to read 0 / 2 Behind a paywall — scores zero
Points 62 / 96 Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 62 of the 96 points we could judge it on is 65 out of 100.
Total 65 / 100 —

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

Read the original

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