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Related Experiment Videos

Aβ-induced vulnerability propagates via the brain's default mode network.

Tharick A Pascoal1,2, Sulantha Mathotaarachchi1, Min Su Kang1,2

  • 1Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, H4H 1R3, Montreal, Canada.

Nature Communications
|June 6, 2019
PubMed
Summary

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Brain amyloid-β (Aβ) aggregation causes distant brain hypometabolism, which, when interacting with local Aβ, drives dementia progression. This mechanism is independent of neurofibrillary tangles, offering new insights into Alzheimer's disease.

Area of Science:

  • Neuroscience
  • Alzheimer's Disease Research
  • Metabolic Imaging

Background:

  • The relationship between brain amyloid-β (Aβ) deposition, glucose metabolism, and dementia symptoms is crucial for understanding Alzheimer's disease (AD).
  • Existing research highlights Aβ plaques and neurofibrillary tangles as key pathological hallmarks of AD.
  • The precise mechanisms linking Aβ pathology to metabolic dysfunction and cognitive decline require further elucidation.

Purpose of the Study:

  • To investigate the causal link between amyloid-β aggregation in the default mode network and regional brain hypometabolism.
  • To determine if the interaction between hypometabolism and local Aβ aggregation predicts cognitive decline in Alzheimer's disease.
  • To validate these findings in an animal model lacking neurofibrillary tangles.

Main Methods:

Related Experiment Videos

  • Positron emission tomography (PET) imaging using [18F]florbetapir for Aβ and [18F]FDG for glucose metabolism.
  • Application of a novel analytical framework to assess Aβ-induced hypometabolism and its functional connectivity.
  • Utilized transgenic Aβ rats as a model to study Aβ-related pathology independent of tau.

Main Results:

  • Aβ aggregation in the default mode network was found to induce hypometabolism in functionally connected, distant brain regions.
  • An interaction between regional hypometabolism and overlapping Aβ deposition significantly correlated with subsequent cognitive decline.
  • These Aβ-dependent effects on metabolism and cognition were confirmed in Aβ rats, irrespective of neurofibrillary tangle formation.

Conclusions:

  • Aβ pathology can induce remote metabolic dysfunction through interconnected brain networks.
  • The interplay between Aβ-driven metabolic vulnerability and local Aβ accumulation accelerates dementia progression.
  • This study proposes a novel mechanism for cognitive deterioration in Alzheimer's disease, independent of neurofibrillary tangles.