Evidence map›Paper›PMID 35931678›Full record

ArticleNature communications2022

Multi-cohort and longitudinal Bayesian clustering study of stage and subtype in Alzheimer's disease.

Konstantinos Poulakis, Joana B Pereira, J-Sebastian Muehlboeck, Lars-Olof Wahlund, Örjan Smedby, Giovanni Volpe, Colin L Masters, David Ames, Yoshiki Niimi, Takeshi Iwatsubo and 4 more

Erratum issuedAbstract 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. An erratum has been issued. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing 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

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

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  8. Multimodal axes reveal individualized amyloid-medRxiv : the preprint server for health sciences · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Konstantinos PoulakisDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden. konstantinos.poulakis@ki.se.ORCID http://orcid.org/0000-0002-6600-8086
Joana B PereiraDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
J-Sebastian MuehlboeckDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Lars-Olof WahlundDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.
Örjan SmedbyDepartment of Biomedical Engineering and Health Systems (MTH), KTH Royal Institute of Technology, Stockholm, Sweden.
Giovanni VolpeDepartment of Physics, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0001-5057-1846
Colin L MastersThe Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Victoria, Australia.
David AmesAcademic Unit for Psychiatry of Old Age, St George's Hospital, University of Melbourne, Melbourne, Victoria, Australia.
Yoshiki NiimiUnit for Early and Exploratory Clinical Development, The University of Tokyo Hospital, Tokyo, Japan.
Takeshi IwatsuboUnit for Early and Exploratory Clinical Development, The University of Tokyo Hospital, Tokyo, Japan.
Daniel FerreiraDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0001-9522-4338
Eric WestmanDivision of Clinical Geriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-3115-2977
Japanese Alzheimer’s Disease Neuroimaging Initiative
Australian Imaging, Biomarkers and Lifestyle study

Funding

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

Abstract

Understanding Alzheimer's disease (AD) heterogeneity is important for understanding the underlying pathophysiological mechanisms of AD. However, AD atrophy subtypes may reflect different disease stages or biologically distinct subtypes. Here we use longitudinal magnetic resonance imaging data (891 participants with AD dementia, 305 healthy control participants) from four international cohorts, and longitudinal clustering to estimate differential atrophy trajectories from the age of clinical disease onset. Our findings (in amyloid-β positive AD patients) show five distinct longitudinal patterns of atrophy with different demographical and cognitive characteristics. Some previously reported atrophy subtypes may reflect disease stages rather than distinct subtypes. The heterogeneity in atrophy rates and cognitive decline within the five longitudinal atrophy patterns, potentially expresses a complex combination of protective/risk factors and concomitant non-AD pathologies. By alternating between the cross-sectional and longitudinal understanding of AD subtypes these analyses may allow better understanding of disease heterogeneity.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAtrophyBayes TheoremBrainCluster AnalysisCross-Sectional StudiesHumansLongitudinal StudiesMagnetic Resonance Imaging

Identifiers

PMID35931678
PMCPMC9355993

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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.