• adenylyl cyclase;
  • Alzheimer's disease;
  • β-amyloid;
  • G-protein;
  • phospholipase C;
  • protein kinase C;
  • neurotransmitters;
  • receptors

It has long been assumed that widespread changes in postsynaptic neurotransmitter receptor function are not a feature of the disrupted neurotransmission seen in the brains with Alzheimer's disease (AD). However, recent evidence from postmortem brain and fibroblast studies suggests that both the neurotransmitter receptor/G-protein-modulated adenylyl cyclase and the phosphatidylinositol hydrolysis signal transduction cascades are disrupted in AD. Such disruptions may severely limit the functional integrity of key receptor types and undermine pharmacological attempts to ameliorate disease symptomatology through neurotransmitter replacement strategies. The involvement of some signalling mechanisms in the regulation of β-amyloid precursor protein metabolism suggests also that disrupted signal transduction may exacerbate AD pathology.