From Acetylcholine to Amyloid: Neurotransmitters and the Pathology of Alzheimer's Disease

Abstract

Brain amyloid deposits play a central role in the histopathology of Alzheimer's disease (AD), as evidenced by increased formation of amyloid β peptides (Aβ) in genetic forms of AD that are caused by mutations in the presenilin genes, or the amyloid β protein precursor (APP) gene. Neuronal deafferentation in AD brain may also be associated with accelerated Aβ 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 Aβ formation.