Evidence map›Paper›PMID 33495928›Full record

ArticleEuropean journal of nuclear medicine and molecular imaging2021

Relationship between amyloid and tau levels and its impact on tau spreading.

Vincent Doré, Natasha Krishnadas, Pierrick Bourgeat, Kun Huang, Shenpeng Li, Samantha Burnham, Colin L Masters, Jurgen Fripp, Victor L Villemagne, Christopher C Rowe

Open access · hybridAbstract read
In one paragraph

Article in European journal of nuclear medicine and molecular imaging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
12.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 100 citations in OpenAlex.

  1. Trial
  2. Evaluation of tau deposition usingAlzheimer's research & therapy · 2022
    Trial
  3. The clinical Alzheimer's disease spectrum classified in the A/T/N framework withEuropean journal of nuclear medicine and molecular imaging · 2026
    Observational
  4. Classification of tau status with machine learning models in amyloid-positive cohorts.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Night-to-night rapid eye movement sleep variability: A relevant marker of early amyloid-β deposition.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Observational
  10. Article
  11. The relationships between ethnoracial identity, Aβ positivity, APOEε4, and medial temporal lobe tau PET.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  12. Article
  13. DynamicalbioRxiv : the preprint server for biology · 2026
    Article
  14. Characterizing amyloid and tau positron emission tomography-based stages across the clinical continuum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  15. Article
  16. Spatial patterns of tau accumulation across the Alzheimer's disease spectrum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  17. Mesial temporal tau pathology impacts basal forebrain degeneration in early Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  18. Multivariate models using NULISAseq and plasma p-tau217 for staging Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Vincent DoréHealth and Biosecurity Flagship, The Australian eHealth Research Centre, Melbourne, Victoria, Australia. Vincent.Dore@csiro.au.ORCID http://orcid.org/0000-0002-8051-0558
Natasha KrishnadasDepartment of Molecular Imaging & Therapy, Austin Health, LVL1 Harrold STOKES Block, 145 Studley Road, Heidelberg, Melbourne, Victoria, 3084, Australia.
Pierrick BourgeatHealth and Biosecurity Flagship, The Australian eHealth Research Centre, Brisbane, Queensland, Australia.
Kun HuangDepartment of Molecular Imaging & Therapy, Austin Health, LVL1 Harrold STOKES Block, 145 Studley Road, Heidelberg, Melbourne, Victoria, 3084, Australia.
Shenpeng LiHealth and Biosecurity Flagship, The Australian eHealth Research Centre, Melbourne, Victoria, Australia.
Samantha BurnhamHealth and Biosecurity Flagship, The Australian eHealth Research Centre, Melbourne, Victoria, Australia.
Colin L MastersThe Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria, Australia.
Jurgen FrippHealth and Biosecurity Flagship, The Australian eHealth Research Centre, Brisbane, Queensland, Australia.
Victor L VillemagneDepartment of Molecular Imaging & Therapy, Austin Health, LVL1 Harrold STOKES Block, 145 Studley Road, Heidelberg, Melbourne, Victoria, 3084, Australia.
Christopher C RoweDepartment of Molecular Imaging & Therapy, Austin Health, LVL1 Harrold STOKES Block, 145 Studley Road, Heidelberg, Melbourne, Victoria, 3084, Australia.
Australian e-Health Research Centre · AUThe University of Melbourne · AUAustin Health · AU

Funding

National Health and Medical Research Council APP1132604National Health and Medical Research Council APP1140853National Health and Medical Research Council APP1152623
6 · The paper itself

Abstract

purposePrevious studies have shown that Aβ-amyloid (Aβ) likely promotes tau to spread beyond the medial temporal lobe. However, the Aβ levels necessary for tau to spread in the neocortex is still unclear.

methodsFour hundred sixty-six participants underwent tau imaging with [18F]MK6420 and Aβ imaging with [

resultsThe plots of prevalence of T+ show earlier and greater increase along the Centiloid continuum in the medial temporal area compared to neocortex. Prevalence of T+ was low but associated with Aβ level between 10 and 40 CL reaching 23% in Me, 15% in Te, and 11% in R. Between 40 and 70 CL, the prevalence of T+ subjects per CL increased fourfold faster and at 70 CL was 64% in Me, 51% in Te, and 37% in R. In cognitively unimpaired, there were no T+ in R below 50 CL. The highest prevalence of T+ were found in the entorhinal cortex, reaching 40% at 40 CL and 80% at 60 CL.

conclusionOutside the entorhinal cortex, abnormal levels of cortical tau on PET are rarely found with Aβ below 40 CL. Above 40 CL prevalence of T+ accelerates in all areas. Moderate Aβ levels are required before abnormal neocortical tau becomes detectable.

Indexed as

Alzheimer Diseasetau ProteinsAmyloidAmyloid beta-PeptidesHumansMagnetic Resonance ImagingPositron-Emission TomographyAmyloidAmyloid beta-Peptidestau ProteinsAlzheimer’s diseaseAβ-amyloid imagingNeurodegenerationPositron emission tomographyTau imagingTauopathies

Identifiers

PMID33495928
PMCPMC8175299
OpenAlexW3124134315

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.