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Antidepressants and bladder antimuscarinics increase dementia risk by causing neurotoxicity and altering amyloid-beta peptide processing. These common anticholinergic drugs directly impact neuronal function, contributing to Alzheimer's disease development.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Stem Cell Biology

Background:

  • Anticholinergic medications are widely used by older adults.
  • Evidence links certain anticholinergics (antidepressants, bladder antimuscarinics) to increased dementia risk.
  • Confounding by indication complicates direct causal links.

Purpose of the Study:

  • To investigate the direct effects of anticholinergic drugs on dementia-related cellular phenotypes.
  • To elucidate the molecular mechanisms by which these drugs affect neuronal function.

Main Methods:

  • Generated 16 human induced pluripotent stem cell (hiPSC) lines from Adult Changes in Thought (ACT) participants.
  • Differentiated hiPSC lines into cortical neurons (hiPSC-Ns).
  • Treated hiPSC-Ns with antidepressants, bladder antimuscarinics, antihistamines, and antispasmodics at varying concentrations and timepoints; assessed neurotoxicity, amyloid-beta (Aβ) peptide ratios, and tau phosphorylation.

Main Results:

  • Antidepressants and bladder antimuscarinics induced dose- and time-dependent neurotoxicity.
  • These drug classes increased the Aβ42/Aβ40 ratio, indicating pathogenic amyloid precursor protein processing.
  • Oxybutynin showed the highest Aβ42/Aβ40 ratio increase; no changes in tau phosphorylation were observed.

Conclusions:

  • Antidepressants and bladder antimuscarinics induce neurotoxicity and pathogenic Aβ secretion.
  • Findings validate a direct link between these anticholinergic drugs and dementia risk.
  • The study provides molecular insights into drug-induced neuronal dysfunction contributing to Alzheimer's disease.