Comparison of Amyloid β and Tau Spread Models in Alzheimer's Disease

Hang Rai Kim, Peter Lee, Sang Won Seo, Jee Hoon Roh, Minyoung Oh, Jungsu S. Oh, Seung Jun Oh, Jae Seung Kim, Yong Jeong

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)


Tau and amyloid β (Aβ), 2 key pathogenic proteins in Alzheimer's disease (AD), reportedly spread throughout the brain as the disease progresses. Models of how these pathogenic proteins spread from affected to unaffected areas had been proposed based on the observation that these proteins could transmit to other regions either through neural fibers (transneuronal spread model) or through extracellular space (local spread model). In this study, we modeled the spread of tau and Aβ using a graph theoretical approach based on resting-state functional magnetic resonance imaging. We tested whether these models predict the distribution of tau and Aβ in the brains of AD spectrum patients. To assess the models' performance, we calculated spatial correlation between the model-predicted map and the actual map from tau and amyloid positron emission tomography. The transneuronal spread model predicted the distribution of tau and Aβ deposition with significantly higher accuracy than the local spread model. Compared with tau, the local spread model also predicted a comparable portion of Aβ deposition. These findings provide evidence of transneuronal spread of AD pathogenic proteins in a large-scale brain network and furthermore suggest different contributions of spread models for tau and Aβ in AD.

Original languageEnglish
Pages (from-to)4291-4302
Number of pages12
JournalCerebral Cortex
Issue number10
Publication statusPublished - 2019 Sept 13
Externally publishedYes


  • Alzheimer's disease
  • amyloid β
  • positron emission tomography
  • resting-state functional magnetic resonance imaging
  • tau

ASJC Scopus subject areas

  • Cognitive Neuroscience
  • Cellular and Molecular Neuroscience


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