Evidence map›Paper›PMID 40913038›Full record

ArticleNature communications2025

Hemispheric asymmetry of tau pathology is related to asymmetric amyloid deposition in Alzheimer's Disease.

Toomas Erik Anijärv, Rik Ossenkoppele, Ruben Smith, Alexa Pichet Binette, Lyduine E Collij, Harry H Behjat, Jonathan Rittmo, Linda Karlsson, Khazar Ahmadi, Olof Strandberg and 8 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

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

  1. Pooled it
  2. Article
  3. Visual versus quantitative tau-PET Braak staging in Alzheimer's disease using [European journal of nuclear medicine and molecular imaging · 2026
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  9. DynamicalbioRxiv : the preprint server for biology · 2026
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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

18 authors.

Toomas Erik AnijärvClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden. toomas_erik.anijarv@med.lu.se.ORCID http://orcid.org/0000-0002-3650-4230
Rik OssenkoppeleClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0003-1584-7477
Ruben SmithClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-7147-0112
Alexa Pichet BinetteClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-5218-3337
Lyduine E CollijClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-6263-1762
Harry H BehjatClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-6729-6801
Jonathan RittmoSciLifeLab, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-5075-0166
Linda KarlssonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-0630-772X
Khazar AhmadiDepartment of Neuropsychology, Ruhr University Bochum, Bochum, Germany.ORCID http://orcid.org/0000-0002-3371-6211
Olof StrandbergClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.
Alzheimer’s Disease Neuroimaging Initiative
Danielle van WestenDiagnostic Radiology, Institution for Clinical Sciences, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-8649-9874
Jacob W VogelSciLifeLab, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0001-6394-9940
Erik StomrudClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.
Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-9267-1930
Niklas Mattsson-CarlgrenClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden.ORCID http://orcid.org/0000-0002-8885-7724
Nicola SpotornoClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden. nicola.spotorno@med.lu.se.ORCID http://orcid.org/0000-0001-5404-8788
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Faculty of Medicine, Lund University, Lund, Sweden. oskar.hansson@med.lu.se.ORCID http://orcid.org/0000-0001-8467-7286

Funding

Project 1U19AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI MONICA G. RIVERA-MINDT · 2016 to 2026
$226.7M
NIA NIH HHS U19 AG024904
6 · The paper itself

Abstract

The distribution of tau pathology in Alzheimer's disease (AD) shows remarkable inter-individual heterogeneity, including hemispheric asymmetry. However, the factors driving this asymmetry remain poorly understood. Here we explore whether tau asymmetry is linked to i) reduced inter-hemispheric brain connectivity (potentially restricting tau spread), or ii) asymmetry in amyloid-beta (Aβ) distribution (indicating greater hemisphere-specific vulnerability to AD pathology). We include 452 participants from the Swedish BioFINDER-2 cohort with evidence of both Aβ pathology (CSF Aβ42/40 or neocortical Aβ-PET) and tau pathology (temporal tau-PET), categorising them as left asymmetric (n = 102), symmetric (n = 306), or right asymmetric (n = 44) based on temporal lobe tau-PET uptake distribution. We assess edge-wise inter-hemispheric functional (RSfMRI; n = 318) and structural connectivity (dMRI; n = 352) but find no association between tau asymmetry and connectivity. In contrast, we observe a strong association between tau and Aβ laterality patterns based on PET uptake (n = 233; β = 0.632, p < 0.001), which we replicate in three independent cohorts (n = 234; β = 0.535, p < 0.001). In a longitudinal Aβ-positive sample, we show that baseline Aβ asymmetry predicts progression of tau laterality over time (n = 289; β = 0.025, p = 0.028). These findings suggest that tau asymmetry is not associated with a weaker inter-hemispheric connectivity but might reflect hemispheric differences in vulnerability to Aβ pathology, underscoring the role of regional vulnerability in determining the distribution of AD pathology.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBraintau ProteinsAgedAged, 80 and overCohort StudiesFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedPeptide FragmentsPositron-Emission TomographyTemporal LobeAmyloid beta-PeptidesPeptide Fragmentstau Proteins

Identifiers

PMID40913038
PMCPMC12413461

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.