Evidence map›Paper›PMID 36814346›Full record

ArticleAlzheimer's research & therapy2023

Associations between different tau-PET patterns and longitudinal atrophy in the Alzheimer's disease continuum: biological and methodological perspectives from disease heterogeneity.

Rosaleena Mohanty, Daniel Ferreira, Agneta Nordberg, Eric Westman, Alzheimer’s Disease Neuroimaging Initiative

Erratum issuedAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–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

23 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Personalizing progressive changes to brain structure in Alzheimer's disease using normative modeling.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Personalising Alzheimer's Disease progression using brain atrophy markers.medRxiv : the preprint server for health sciences · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Rosaleena MohantyDivision of Clinical Geriatrics, Center for Alzheimer Research. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Blickagången 16, 14152, Huddinge, Sweden. rosaleena.mohanty@ki.se.
Daniel FerreiraDivision of Clinical Geriatrics, Center for Alzheimer Research. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Blickagången 16, 14152, Huddinge, Sweden.
Agneta NordbergDivision of Clinical Geriatrics, Center for Alzheimer Research. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Blickagången 16, 14152, Huddinge, Sweden.
Eric WestmanDivision of Clinical Geriatrics, Center for Alzheimer Research. Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Blickagången 16, 14152, Huddinge, Sweden.
Alzheimer’s Disease Neuroimaging Initiative

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
NIA NIH HHS U01 AG024904
6 · The paper itself

Abstract

backgroundSubtypes and patterns are defined using tau-PET (tau pathology) and structural MRI (atrophy) in Alzheimer's disease (AD). However, the relationship between tau pathology and atrophy across these subtypes/patterns remains unclear. Therefore, we investigated the biological association between baseline tau-PET patterns and longitudinal atrophy in the AD continuum; and the methodological characterization of heterogeneity as a continuous phenomenon over the conventional discrete subgrouping.

methodsIn 366 individuals (amyloid-beta-positive cognitively normal, prodromal AD, AD dementia; amyloid-beta-negative cognitively normal), we examined the association between tau-PET patterns and longitudinal MRI. We modeled tau-PET patterns as a (a) continuous phenomenon with key dimensions: typicality and severity; and (b) discrete phenomenon by categorization into patterns: typical, limbic predominant, cortical predominant and minimal tau. Tau-PET patterns and associated longitudinal atrophy were contextualized within the Amyloid/Tau/Neurodegeneration (A/T/N) biomarker scheme.

resultsLocalization and longitudinal atrophy change vary differentially across different tau-PET patterns in the AD continuum. Atrophy, a downstream event, did not always follow a topography akin to the corresponding tau-PET pattern. Further, heterogeneity as a continuous phenomenon offered an alternative and useful characterization, sharing correspondence with the conventional subgrouping. Tau-PET patterns also show differential A/T/N profiles.

conclusionsThe site and rate of atrophy are different across the tau-PET patterns. Heterogeneity should be treated as a continuous, not discrete, phenomenon for greater sensitivity. Pattern-specific A/T/N profiles highlight differential multimodal interactions underlying heterogeneity. Therefore, tracking multimodal interactions among biomarkers longitudinally, modeling disease heterogeneity as a continuous phenomenon, and examining heterogeneity across the AD continuum could offer avenues for precision medicine.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloidAmyloid beta-PeptidesAmyloidogenic ProteinsAtrophyBiomarkersHumansMagnetic Resonance ImagingPositron-Emission Tomographytau ProteinsAmyloidAmyloid beta-PeptidesAmyloidogenic ProteinsBiomarkerstau ProteinsAlzheimer’s disease continuumHeterogeneityLongitudinal MRIPatternsSubtypesTau-PET

Identifiers

PMID36814346
PMCPMC9945609

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.