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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
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Elevation in network dynamics amplifies amyloid-dependent tau pathology.

Jieying Li1,2,3, Yang Yi2, Lin Gan4

  • 1Translational Neuroimaging Laboratory Department of Neurology and Neurosurgery, McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|April 14, 2026
PubMed
Summary
This summary is machine-generated.

Increased brain network switching is linked to amyloid beta and tau pathology in Alzheimer's disease, potentially accelerating cognitive decline. This highlights network dynamics as a key factor in disease progression.

Keywords:
Alzheimer's diseaseBraak stagingbrain networkcognitionpathology

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Area of Science:

  • Neuroscience
  • Biomarkers of Aging and Dementia
  • Neuroimaging

Background:

  • The relationship between brain network dynamics and Alzheimer's disease (AD) pathologies, including amyloid beta (Aβ) and tau, across different disease stages (Braak stages) is not well understood.
  • Investigating these connections is crucial for understanding AD pathogenesis and progression.

Purpose of the Study:

  • To investigate the association between brain network dynamics, Aβ and tau pathology, and cognitive status in a cohort of aging individuals.
  • To explore how network switching rates relate to the accumulation of Aβ and tau and their impact on cognitive function.

Main Methods:

  • A cross-sectional study involving 216 participants from the Translational Biomarkers of Aging and Dementia (TRIAD) cohort.
  • Resting-state functional magnetic resonance imaging (rs-fMRI) was analyzed using a multilayer modularity algorithm to assess brain network dynamics.
  • Participants were stratified based on amyloid and tau positron emission tomography (PET) biomarkers and Braak stages.

Main Results:

  • Individuals with both Aβ and tau positivity exhibited significantly higher network switching rates compared to those negative for both.
  • Network switching rates increased progressively with advancing Braak stages and correlated with Aβ and tau burden in specific brain networks (dorsal attention, sensorimotor).
  • A significant interaction between network switching rate and Aβ burden was observed, synergistically accelerating tau accumulation in Braak stages III-V and correlating with cognitive severity.

Conclusions:

  • Elevated brain network switching is associated with increased Aβ and tau pathology and cognitive deterioration in Alzheimer's disease.
  • These findings suggest that increased network switching may exacerbate Aβ-related tau accumulation and cognitive decline, supporting a framework where network dynamics play a critical role in AD progression.