{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Anijarv TE"],"funding":["European Research Council"],"pagination":["8232"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12413461"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_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."],"journal":["Nature communications"],"pubmed_title":["Hemispheric asymmetry of tau pathology is related to asymmetric amyloid deposition in Alzheimer's Disease."],"pmcid":["PMC12413461"],"funding_grant_id":["101096455"],"pubmed_authors":["Strandberg O","Karlsson L","Vogel JW","Beckett L","Jack CR","Landau S","Toga AW","Alzheimer’s Disease Neuroimaging Initiative","Rivera-Mindt M","Okonkwo O","Green RC","Perrin RJ","Jagust W","Saykin AJ","Aisen P","Palmqvist S","Hansson O","van Westen D","Weiner M","Pichet Binette A","Spotorno N","Ossenkoppele R","Stomrud E","Ahmadi K","Rittmo J","Tosun D","Smith R","Behjat HH","Anijarv TE","Collij LE","Mattsson-Carlgren N","Shaw LM","Lee EB","Nho K","Harvey D","Petersen R"],"additional_accession":[]},"is_claimable":false,"name":"Hemispheric asymmetry of tau pathology is related to asymmetric amyloid deposition in Alzheimer's Disease.","description":"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.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-29T22:24:49.468Z","creation":"2026-04-08T06:12:34.284Z"},"accession":"S-EPMC12413461","cross_references":{"pubmed":["40913038"],"doi":["10.1038/s41467-025-63564-2"]}}