Regional Aβ-tau interactions promote onset and acceleration of Alzheimer's disease tau spreading

Alzheimer's Disease Neuroimaging Initiative

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)


Amyloid-beta and tau are key molecules in the pathogenesis of Alzheimer's disease, but it remains unclear how these proteins interact to promote disease. Here, by combining cross-sectional and longitudinal molecular imaging and network connectivity analyses in living humans, we identified two amyloid-beta/tau interactions associated with the onset and propagation of tau spreading. First, we show that the lateral entorhinal cortex, an early site of tau neurofibrillary tangle formation, is subject to remote, connectivity-mediated amyloid-beta/tau interactions linked to initial tau spreading. Second, we identify the inferior temporal gyrus as the region featuring the greatest local amyloid-beta/tau interactions and a connectivity profile well suited to accelerate tau propagation. Taken together, our data address long-standing questions regarding the topographical dissimilarity between early amyloid-beta and tau deposition.

Original languageEnglish
Pages (from-to)1932-1943.e5
Issue number12
Publication statusPublished - 2022 Jun 15


  • Alzheimer's disease
  • DTI
  • PET
  • amyloid-beta
  • connectome
  • tau

ASJC Scopus subject areas

  • Neuroscience(all)


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