Evidence map›Paper›PMID 31894103›Full record

Observational studyScience translational medicine2020

Prospective longitudinal atrophy in Alzheimer's disease correlates with the intensity and topography of baseline tau-PET.

Renaud La Joie, Adrienne V Visani, Suzanne L Baker, Jesse A Brown, Viktoriya Bourakova, Jungho Cha, Kiran Chaudhary, Lauren Edwards, Leonardo Iaccarino, Mustafa Janabi and 12 more

Open access · greenAbstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Science translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 389 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
389citing papers in PubMed, 4 pooled it
43.9field-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

389 citing papers in PubMed, 4 syntheses or guidelines pooled it, 598 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Guideline
  4. Pooled it
  5. Trial
  6. Trial
  7. Article
  8. Brain microstructure mediates the relationship between Alzheimer's proteinopathies and memory.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  9. Network-dependent remote effects and local tau burden jointly shape neuronal dysfunction in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Visual versus quantitative tau-PET Braak staging in Alzheimer's disease using [European journal of nuclear medicine and molecular imaging · 2026
    Article
  16. Article
  17. Article
  18. Article
  19. Modular brain networks shape amyloid-driven tau spread and cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  20. Article

329 more citing papers are in PubMed but not listed here.

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

22 authors at 2 institutions in 1 country.

Renaud La JoieMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA. renaud.lajoie@ucsf.edu.ORCID 0000-0003-2581-8100
Adrienne V VisaniMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-5379-3687
Suzanne L BakerMolecular Biophysics and Integrated Bioimaging Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.
Jesse A BrownMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-3139-9451
Viktoriya BourakovaMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Jungho ChaMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0003-1189-2051
Kiran ChaudharyMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-0252-4129
Lauren EdwardsMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-8434-9669
Leonardo IaccarinoMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0003-0053-9519
Mustafa JanabiMolecular Biophysics and Integrated Bioimaging Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.ORCID 0000-0003-0134-0317
Orit H Lesman-SegevMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Zachary A MillerMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
David C PerryMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
James P O'NeilMolecular Biophysics and Integrated Bioimaging Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.ORCID 0000-0002-4980-4240
Julie PhamMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Julio C RojasMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-1308-646X
Howard J RosenMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
William W SeeleyMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Richard M TsaiMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0003-2784-7992
Bruce L MillerMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.ORCID 0000-0002-2152-4220
William J JagustMolecular Biophysics and Integrated Bioimaging Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.ORCID 0000-0002-4458-113X
Gil D RabinoviciMemory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
University of California, San Francisco · USLawrence Berkeley National Laboratory · US

Funding

Early Onset AD Consortium - the LEAD Study (LEADS)U01AG057195 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI APOSTOLOVA, LIANA G, CARRILLO, MARIA C · 2018 to 2023
$70.3M
TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI BRUCE L MILLER · 2002 to 2026
$67.2M
Research Education ComponentP30AG062422 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HOWARD J ROSEN · 2019 to 2026
$36.9M
PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
The Four Repeat Tauopathy Neuroimaging InitiativeR01AG038791 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2010 to 2020
$18.1M
Neural and Biochemical Mechanisms of Cognitive AgingR01AG034570 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI William J. Jagust · 2009 to 2026
$12.0M
The Frontotemporal Lobar Degeneration Neuroimaging InitiativeR01AG032306 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSEN, HOWARD J · 2009 to 2013
$10.0M
Multidisciplinary Research Fellowship in Alzheimer’s disease and Related DementiasT32AG023481 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRUCE L MILLER, HOWARD J ROSEN · 2005 to 2026
$7.4M
Early Age-of-Onset AD: Clinical Heterogeneity and Network DegenerationR01AG045611 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RABINOVICI, GIL DAN · 2014 to 2018
$3.1M
Multimodal Imaging in Frontotemporal DegenerationK24AG045333 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSEN, HOWARD J · 2013 to 2023
$1.9M
Proteomics for fluid biomarker discovery in frontotemporal dementiaK23AG059888 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROJAS-MARTINEZ, JULIO CESAR · 2019 to 2023
$995k
Reward processing in frontotemporal dementiaK23AG045289 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PERRY, DAVID C · 2014 to 2018
$880k
NIA NIH HHS K01 AG055698NIA NIH HHS K23 AG045289NIA NIH HHS K23 AG059888NIA NIH HHS K24 AG045333NIA NIH HHS P01 AG019724NIA NIH HHS P30 AG062422NIA NIH HHS P50 AG023501NIA NIH HHS R01 AG032306NIA NIH HHS R01 AG034570NIA NIH HHS R01 AG038791NIA NIH HHS R01 AG045611NIA NIH HHS T32 AG023481NIA NIH HHS U01 AG057195
6 · The paper itself

Abstract

β-Amyloid plaques and tau-containing neurofibrillary tangles are the two neuropathological hallmarks of Alzheimer's disease (AD) and are thought to play crucial roles in a neurodegenerative cascade leading to dementia. Both lesions can now be visualized in vivo using positron emission tomography (PET) radiotracers, opening new opportunities to study disease mechanisms and improve patients' diagnostic and prognostic evaluation. In a group of 32 patients at early symptomatic AD stages, we tested whether β-amyloid and tau-PET could predict subsequent brain atrophy measured using longitudinal magnetic resonance imaging acquired at the time of PET and 15 months later. Quantitative analyses showed that the global intensity of tau-PET, but not β-amyloid-PET, signal predicted the rate of subsequent atrophy, independent of baseline cortical thickness. Additional investigations demonstrated that the specific distribution of tau-PET signal was a strong indicator of the topography of future atrophy at the single patient level and that the relationship between baseline tau-PET and subsequent atrophy was particularly strong in younger patients. These data support disease models in which tau pathology is a major driver of local neurodegeneration and highlight the relevance of tau-PET as a precision medicine tool to help predict individual patient's progression and design future clinical trials.

Indexed as

Positron-Emission TomographyAgedAged, 80 and overAlzheimer DiseaseAtrophyCarbolinesCerebral CortexFemaleFollow-Up StudiesHumansLongitudinal StudiesMaleMiddle Agedtau Proteins7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indoleCarbolinestau Proteins

Identifiers

PMID31894103
PMCPMC7035952
OpenAlexW2998707549

What OpenQuestion holds

Textmetadata
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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.