Regulation of APP processing. Potential for the therapeutical reduction of brain amyloid burden.

Annals of the New York Academy of Sciences 1996

["Nitsch R M", "Wurtman R J", "Growdon J H"]

Abstract

The role of brain amyloid in the pathogenesis of Alzheimer’s disease (AD) is discussed controversially, but combined genetic and biochemical evidence points to a central role of the gene encoding the amyloid precursor APP in at least some forms of AD. This article proposes that preventing brain amyloid formation is a rational concept for drug treatment of AD. We suggest that pharmacologically active ligands for specific cell surface receptor subtypes--normally stimulated by neurotransmitters, growth factors, and cytokines--constitute a class of chemicals that might be useful to accelerate processing of APP into non-amyloidogenic, and biologically active, derivatives. This class of agents includes muscarinic m1 and m3 agonists, serotoninergic 5-HT2a and 5-HT2c agonists, glutamatergic mGluR1 agonists, as well as agonists for bradykinin and vasopressin receptors.

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