Quantity and Quality Changes of G Protein in Dementia of the Alzheimer Type
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
KeywordsAdenylate Cyclase Protein Subunit Adenylate Cyclase Activity Synaptic Membrane Brain Membrane
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