Quantity and Quality Changes of G Protein in Dementia of the Alzheimer Type

Abstract

Changes in many neurotransmitters, their synthetic enzymes and their receptors-binding sites have been demonstrated in the brains of Alzheimer’s disease.¹ However, alterations in presynaptic neurotransmitters or receptor binding are not necessarily linked to disturbances in the cell signaling system such as the coupling interaction of receptor-transducer molecules - - effectors that produce the second messenger. Therefore, recent studies have focused on post-receptor signal transduction in this disease. Several lines of research have suggested that disturbances of post-receptor signal transduction in two major second messenger systems are composed of cyclic AMP production by the enzyme adenylate cyclase and phosphoinositide (PI) hydrolysis by phospholipase C in Alzheimer’s disease. For example, changes of the coupling of muscarinic receptors to G protein, and reduction of receptor agonist or GTP analog stimulated adenylate cyclase, changed redistribution of protein kinase C and reduced phosphoinositide have been reported.¹