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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 69 out of 100. Caregiving

Topic: Amyloid, tau and blood-test diagnosis

Advances in molecular positron emission tomography (PET) have enabled anatomic tracking of brain pathology in longitudinal studies of normal aging and dementia, including assessment of the central model of Alzheimer's disease (AD) pathogenesis, according to which TAU pathology begins focally but expands catastrophically under the influence of amyloid-β (Aβ) pathology to mediate neurodegeneration and cognitive decline. Initial TAU deposition occurs many years before Aβ in a specific area of the medial temporal lobe. Building on recent work that enabled focus of molecular PET measurements on specific TAU-vulnerable convolutional temporal lobe anatomy, we applied an automated anatomic sampling method to quantify TAU PET signal in 443 adult participants from several observational studies of aging and AD, spanning a wide range of ages, Aβ burdens, and degrees of clinical impairment. We detected initial cortical emergence of tauopathy near the rhinal sulcus in clinically normal people and, in a subset with longitudinal 2-year follow-up data ( n = 104), tracked Aβ-associated spread of TAU from this site first to nearby neocortex of the temporal lobe and then to extratemporal regions. Greater rate of TAU spread was associated with baseline measures of both global Aβ burden and medial temporal lobe TAU. These findings are consistent with clinicopathological correlation studies of Alzheimer's tauopathy and enable precise tracking of AD-related TAU progression for natural history studies and prevention therapeutic trials.

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

APA 7th

Sanchez, J. S., Becker, J. A., Jacobs, H. I. L., Hanseeuw, B. J., Jiang, S., Schultz, A. P., et al. (2021). The cortical origin and initial spread of medial temporal tauopathy in Alzheimer's disease assessed with positron emission tomography. Science translational medicine. https://doi.org/10.1126/scitranslmed.abc0655

Vancouver

Sanchez JS, Becker JA, Jacobs HIL, Hanseeuw BJ, Jiang S, Schultz AP, et al. The cortical origin and initial spread of medial temporal tauopathy in Alzheimer's disease assessed with positron emission tomography. Science translational medicine. 2021. doi:10.1126/scitranslmed.abc0655. PMID: 33472953.

BibTeX

@article{sanchez2021-33472953,
  author  = {Sanchez, J. S. and Becker, J. A. and Jacobs, H. I. L. and Hanseeuw, B. J. and Jiang, S. and Schultz, A. P. and Properzi, M. J. and Katz, SR. and others},
  title   = {{The cortical origin and initial spread of medial temporal tauopathy in Alzheimer's disease assessed with positron emission tomography}},
  journal = {Science translational medicine},
  year    = {2021},
  doi     = {10.1126/scitranslmed.abc0655},
  pmid    = {33472953},
  url     = {https://doi.org/10.1126/scitranslmed.abc0655}
}

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

In tau PET scans of 443 adults, tau first appeared near the rhinal sulcus in clinically normal people. In 104 people followed for 2 years, it spread first to nearby temporal-lobe cortex and then beyond the temporal lobe. Faster spread was associated with higher baseline amyloid and medial temporal tau. The study offers a way to track early tau changes in natural-history studies and prevention trials, but it tested no treatment and does not show that amyloid causes the spread.

Study details

How this study scored 69/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 7 of 12; Strength of evidence 3 of 5; Peer-review validation 10 of 10; How recent 3 of 5; Sample size 2 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 4 of 5; Impact for its field and year 4 of 6; Cited by studies here 3 of 6; Still being cited 3 of 4; Senior author's track record 4 of 4; Institution's track record 3 of 3; Multi-centre collaboration 3 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 69 of 100.69 of 100 points earned31 not earned

Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for effect reported and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Science translational medicine)
Journal's citation record 3 / 4 Science Translational Medicine: journal h-index 365 (OpenAlex, 2026-10-29)
Study design 7 / 12 A longitudinal study following the same 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 3 / 5 2021 — within 6 year(s) of the newest study here
Sample size 2 / 4 104 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 200 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 28.6 citations a year over 7 year(s) since 2021
Impact for its field and year 4 / 6 Cited 18.9× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 20 other studies in this library
Still being cited 3 / 4 Cited 102 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 3 / 3 OpenAlex lists 12 institution(s) in 4 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 33472953)
Free to read 0 / 2 Behind a paywall — scores zero
Total 69 / 100 —

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

Read the original

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