Evidence map›Paper›PMID 35393421›Full record

ArticleNature communications2022

A robust and interpretable machine learning approach using multimodal biological data to predict future pathological tau accumulation.

Joseph Giorgio, William J Jagust, Suzanne Baker, Susan M Landau, Peter Tino, Zoe Kourtzi, Alzheimer’s Disease Neuroimaging Initiative

Abstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Solving the 'Goldilocks problem' in dementia clinical trials with multimodal AI.The journal of prevention of Alzheimer's disease · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Global brain activity and its coupling with cerebrospinal fluid flow is related to tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Automatic brain structure segmentation forQuantitative imaging in medicine and surgery · 2023
    Article
  17. Review
  18. Article
  19. Review
  20. Review
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

7 authors.

Joseph GiorgioDepartment of Psychology, University of Cambridge, Cambridge, UK.
William J JagustHelen Wills Neuroscience Institute, University of California, Berkeley, CA, USA.ORCID http://orcid.org/0000-0002-4458-113X
Suzanne BakerMolecular Biophysics & Integrated Bioimaging, Lawrence Berkeley National Laboratory, Berkeley, CA, USA.ORCID http://orcid.org/0000-0003-0209-3127
Susan M LandauHelen Wills Neuroscience Institute, University of California, Berkeley, CA, USA.
Peter TinoSchool of Computer Science, University of Birmingham, Birmingham, UK.
Zoe KourtziDepartment of Psychology, University of Cambridge, Cambridge, UK. zk240@cam.ac.uk.ORCID http://orcid.org/0000-0001-9441-7832
Alzheimer’s Disease Neuroimaging Initiative

Funding

Project 1U19AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MONICA G. RIVERA-MINDT · 2016 to 2026
$226.7M
Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
Neural and Biochemical Mechanisms of Cognitive AgingR01AG034570 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI William J. Jagust · 2009 to 2026
$12.0M
Mechanisms of Alzheimer's Disease Progression in the Aging BrainR01AG062542 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI JAGUST, WILLIAM J. · 2019 to 2023
$4.2M
Biotechnology and Biological Sciences Research Council BB/P021255/1Biotechnology and Biological Sciences Research Council H012508CIHRNIA NIH HHS R01 AG034570NIA NIH HHS R01 AG062542NIA NIH HHS U01 AG024904NIA NIH HHS U19 AG024904Wellcome Trust 205067/Z/16/ZWellcome Trust 209749/Z/17/ZWellcome Trust 221633/Z/20/Z
6 · The paper itself

Abstract

The early stages of Alzheimer's disease (AD) involve interactions between multiple pathophysiological processes. Although these processes are well studied, we still lack robust tools to predict individualised trajectories of disease progression. Here, we employ a robust and interpretable machine learning approach to combine multimodal biological data and predict future pathological tau accumulation. In particular, we use machine learning to quantify interactions between key pathological markers (β-amyloid, medial temporal lobe  atrophy, tau and APOE 4) at mildly impaired and asymptomatic stages of AD. Using baseline non-tau markers we derive a prognostic index that: (a) stratifies patients based on future pathological tau accumulation, (b) predicts individualised regional future rate of tau accumulation, and (c) translates predictions from deep phenotyping patient cohorts to cognitively normal individuals. Our results propose a robust approach for fine scale stratification and prognostication with translation impact for clinical trial design targeting the earliest stages of AD.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesApolipoprotein E4BiomarkersHumansMachine LearningMagnetic Resonance ImagingPositron-Emission Tomographytau ProteinsAmyloid beta-PeptidesApolipoprotein E4Biomarkerstau Proteins

Identifiers

PMID35393421
PMCPMC8989879

What Socratic 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 Socratic graph.