From acetylcholine to amyloid: neurotransmitters and the pathology of Alzheimer's disease

Neurodegeneration. 1996 Dec;5(4):477-82. doi: 10.1006/neur.1996.0066.

Abstract

Brain amyloid deposits play a central role in the histopathology of Alzheimer's disease (AD), as evidenced by increased formation of amyloid beta peptides (A beta) in genetic forms of AD that are caused by mutations in the presenilin genes, or the amyloid beta protein precursor (APP) gene. Neuronal deafferentation in AD brain may also be associated with accelerated A beta formation, because APP processing is regulated by neuronal activity, presumably via several G protein-coupled neurotransmitter receptors. Subtype-selective agonists including muscarinic m1 receptor ligands may be useful for the pharmacological reduction of A beta formation.

Publication types

  • Review

MeSH terms

  • Acetylcholine / metabolism*
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology*
  • Alzheimer Disease / psychology
  • Amyloid / metabolism*
  • Amyloid beta-Protein Precursor / metabolism
  • Amyloid beta-Protein Precursor / physiology
  • Animals
  • Cognition
  • Humans
  • Neurotransmitter Agents / physiology*
  • Protein Processing, Post-Translational

Substances

  • Amyloid
  • Amyloid beta-Protein Precursor
  • Neurotransmitter Agents
  • Acetylcholine