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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. Brain scans and imaging

Topic: Amyloid, tau and blood-test diagnosis

Results Of the 24 individuals, the mean (SD) age was 38.0 (7.4) years, or approximately 6 years younger than the expected onset of clinical symptoms in carriers. Compared with noncarriers, cognitively unimpaired mutation carriers had elevated mean cortical Pittsburgh Compound B distribution volume ratio levels in their late 20s, and 7 of 9 carriers older than 30 years reached the threshold for amyloidosis (distribution volume ratio level > 1.2). In carriers, higher levels of tau deposition were associated with worse performance on the Mini-Mental State Examination (entorhinal cortex: r = -0.60; P = .04; inferior temporal lobe: r = -0.54; P = .06) and the Consortium to Establish a Registry for Alzheimer Disease Word List Delayed Recall (entorhinal cortex: r = -0.86; P Conclusions and relevance The present findings add to the growing evidence that molecular markers can characterize biological changes associated with AD in individuals who are still cognitively unimpaired. The findings also suggest that tau PET imaging may be useful as a biomarker to distinguish individuals at high risk to develop the clinical symptoms of AD and to track disease progression.

Key findings

Why it matters

In this small study of 24 young adults with autosomal dominant Alzheimer disease mutations, carriers showed elevated amyloid in their late 20s, and higher tau deposition was associated with worse performance on some cognitive tests. It suggests these markers may help identify and track people at high risk, but it does not test treating, curing, or preventing the disease.

Study details

How this study scored 60/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 2 of 4; Study design 4 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 2 of 5; Sample size 1 of 4; Effect reported 0 of 3; Studied in people 3 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 3 of 3; Multi-centre collaboration 2 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 snapshot of people at one point in time. Scored zero for effect reported and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (JAMA neurology)
Journal's citation record 2 / 4 JAMA Neurology: journal h-index 235 (OpenAlex, 2026-10-29)
Study design 4 / 12 A snapshot of people at one point in time
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 2 / 5 2018 — within 10 year(s) of the newest study here
Sample size 1 / 4 24 participants
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 (participant count stated)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 5 / 7 Cited 187 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 18.7 citations a year over 10 year(s) since 2018
Impact for its field and year 4 / 6 Cited 18.3× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 13 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 / 4 Last-listed author Keith A. Johnson: h-index 127 (OpenAlex, whole career)
Institution's track record 3 / 3 Harvard University: institution h-index 3,235 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 8 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 29435558)
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 →

Read the original

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

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

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.

APA 7th

Quiroz, Y. T., Sperling, R. A., Norton, D. J., Baena, A., Arboleda-Velasquez, J. F., Cosio, D., et al. (2018). Association Between Amyloid and Tau Accumulation in Young Adults With Autosomal Dominant Alzheimer Disease. JAMA neurology. https://doi.org/10.1001/jamaneurol.2017.4907

Vancouver

Quiroz YT, Sperling RA, Norton DJ, Baena A, Arboleda-Velasquez JF, Cosio D, et al. Association Between Amyloid and Tau Accumulation in Young Adults With Autosomal Dominant Alzheimer Disease. JAMA neurology. 2018. doi:10.1001/jamaneurol.2017.4907. PMID: 29435558.

BibTeX

@article{quiroz2018-29435558,
  author  = {Quiroz, Y. T. and Sperling, R. A. and Norton, D. J. and Baena, A. and Arboleda-Velasquez, J. F. and Cosio, D. and Schultz, A. and Lapoint, M. and others},
  title   = {{Association Between Amyloid and Tau Accumulation in Young Adults With Autosomal Dominant Alzheimer Disease}},
  journal = {JAMA neurology},
  year    = {2018},
  doi     = {10.1001/jamaneurol.2017.4907},
  pmid    = {29435558},
  url     = {https://doi.org/10.1001/jamaneurol.2017.4907}
}

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