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Basic Science and Pathogenesis.

Sonia Do Carmo1, Quentin Bonomo1, Joshua T Emmerson1

  • 1McGill University, Montreal, QC, Canada.

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

Advanced tau pathology in Alzheimer's disease exacerbates cholinergic dysfunction by disrupting the nerve growth factor (NGF) pathway. This leads to further degeneration of basal forebrain cholinergic neurons (BFCNs), impacting learning and memory.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • Cholinergic signaling is vital for cognitive functions like learning and memory.
  • Alzheimer's disease (AD) involves degeneration of basal forebrain cholinergic neurons (BFCNs), linked to impaired nerve growth factor (NGF) maturation.
  • Tau pathology's impact on cholinergic dysfunction and the NGF pathway in AD remains unclear.

Purpose of the Study:

  • To investigate how tau pathology influences the NGF metabolic pathway.
  • To determine the effect of tau pathology on cholinergic function in a rat model.

Main Methods:

  • Examined NGF pathway proteins in the cortex and hippocampus of McGill-R955-hTau transgenic rats modeling tauopathy.
  • Assessed NGF pathway protein levels via Western blot and ELISA at 9, 14, and 20 months.
  • Measured cholinergic bouton density (VAChT) and BFCNs (ChAT) in 20-month-old rats.

Main Results:

  • Advanced tauopathy (20 months) showed increased neuroserpin and proNGF, with decreased mature NGF (mNGF).
  • NGF pathway dysregulation was observed later in tau pathology progression.
  • Preliminary findings indicated disrupted NGF pathway components and reduced cholinergic markers, suggesting cholinergic atrophy.

Conclusions:

  • Advanced tauopathy exacerbates the dysregulation of the brain's NGF metabolic pathway.
  • This leads to worsened forebrain cholinergic atrophy in the context of tau pathology.
  • The study highlights a novel mechanism linking tau pathology to cholinergic deficits in AD.