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Amnesia induced in mice by centrally administered beta-amyloid peptides involves cholinergic dysfunction

T Maurice1, B P Lockhart, A Privat

  • 1INSERM U336, Développement, Plasticité et Vieillessement du Système Nerveux, Ecole Nationale Supérieure de Chimie, Montpellier, France.

Brain Research
|January 15, 1996
PubMed
Summary

Beta-amyloid peptide fragments induce Alzheimer's-like memory deficits in mice. Cholinesterase inhibitors and nicotinic agonists reversed these memory impairments, suggesting therapeutic potential.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Alzheimer's disease (AD) is characterized by cognitive deficits linked to beta-amyloid peptide (Aβ) deposition in the brain.
  • The neurotoxic actions of Aβ are hypothesized to be the primary cause of AD-related memory impairment.

Purpose of the Study:

  • To investigate the hypothesis that Aβ deposition causes Alzheimer's-type amnesia.
  • To evaluate the therapeutic potential of cholinergic agents in reversing Aβ-induced memory deficits.

Main Methods:

  • Intracerebroventricular administration of aggregated beta-amyloid (25-35) peptide in mice.
  • Assessment of memory using Y-maze spontaneous alternation, step-down passive avoidance, and water-maze place learning.
  • Evaluation of tacrine (THA) and (-)-nicotine (NIC) effects on memory performance and histological analysis of brain tissue.

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Main Results:

  • Aggregated beta-amyloid (25-35) peptide induced dose-dependent memory impairments in alternation and passive avoidance tasks.
  • Both tacrine and (-)-nicotine dose-dependently reversed the amnesia and improved learning and retention in the water-maze.
  • Histological examination revealed cell loss and amyloid deposits in the cortex and hippocampus of treated mice.

Conclusions:

  • Cerebral deposition of beta-amyloid peptide is strongly associated with learning impairment and cholinergic degeneration.
  • The beta-amyloid (25-35) fragment can induce an Alzheimer's-type amnesia in mice.
  • Cholinergic agents demonstrate potential for treating Aβ-induced cognitive deficits in Alzheimer's disease.