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Basic Science and Pathogenesis.

Kamalini G Ranasinghe1, Kiwamu Kudo1, Faatimah Syed1

  • 1University of California San Francisco, San Francisco, CA, USA.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Alzheimer's disease (AD) involves neural circuit hyperexcitability, with amyloid-beta (Aβ) and tau uniquely linked to different aspects of this dysfunction. Targeting these distinct pathways may improve cognitive outcomes in AD patients.

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Area of Science:

  • Neuroscience
  • Neurology
  • Biomedical Science

Background:

  • Neural circuit hyperexcitability is implicated in Alzheimer's disease (AD) mouse models, linked to amyloid-beta (Aβ) and tau pathology.
  • While epileptiform activity is more common in AD patients, the precise relationship between Aβ, tau, and neural hyperexcitability remains unclear.

Purpose of the Study:

  • To investigate the distinct associations of Aβ and tau with neural circuit hyperexcitability in early-stage AD patients.
  • To differentiate between local synaptic integration deficits (neural hyperactivity) and long-range synaptic input integration deficits (neural fragility).

Main Methods:

  • Magnetoencephalography (MEG) and positron emission tomography (PET) were used in 82 early-stage AD patients and controls.
  • Neural hyperactivity (spectral aperiodic slope) and neural fragility (long-range synaptic input integration) were quantified across 210 cortical regions.
  • Aβ, tau, and neurodegeneration levels were measured and correlated with hyperexcitability metrics.

Main Results:

  • AD patients exhibited increased neural hyperactivity and neural fragility compared to controls.
  • Aβ accumulation correlated with both neural fragility and hyperactivity, while tau correlated only with hyperactivity.
  • Neurodegeneration strongly correlated with hyperactivity, but not fragility. Epileptiform activity in AD patients was associated with increased neural fragility.

Conclusions:

  • Neural circuit hyperexcitability in AD presents diverse manifestations of synaptic integration deficits, distinctly associated with Aβ and tau.
  • Targeting these differential hyperexcitability pathways linked to Aβ and tau may offer novel therapeutic strategies for AD.