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<p>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 &lt; 0.001), which we replicate in three independent cohorts (n = 234; β = 0.535, p &lt; 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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月5日

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  • Toomas Erik Anijärv,
  • Rik Ossenkoppele,
  • Ruben Smith,
  • Alexa Pichet Binette,
  • Lyduine E. Collij,
  • Harry H. Behjat,
  • Jonathan Rittmo,
  • Linda Karlsson,
  • Khazar Ahmadi,
  • Olof Strandberg,
  • Michael Weiner,
  • Paul Aisen,
  • Ronald Petersen,
  • Clifford R. Jack Jr.,
  • William Jagust,
  • Susan Landau,
  • Monica Rivera-Mindt,
  • Ozioma Okonkwo,
  • Leslie M. Shaw,
  • Edward B. Lee,
  • Arthur W. Toga,
  • Laurel Beckett,
  • Danielle Harvey,
  • Robert C. Green,
  • Andrew J. Saykin,
  • Kwangsik Nho,
  • Richard J. Perrin,
  • Duygu Tosun,
  • Danielle van Westen,
  • Jacob W. Vogel,
  • Erik Stomrud,
  • Sebastian Palmqvist,
  • Niklas Mattsson-Carlgren,
  • Nicola Spotorno,
  • Oskar Hansson

摘要

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.