Abstract
Acetyl-CoA provision to the synaptoplasmic comparment of cholinergic nerve terminals plays a regulatory role in the synthesis of acetylcholine. The disturbances in glucose utilization and in decarboxylation of the end product of its matabolism pyruvate, are considered to be significant factors causing cholinergic deficits in several diseases of the central nervous system. In this article we review data concerning role of acetyl-CoA in patomechanisms of disturbances of cholinergic metabolism in Alzheimers disease, thiamine deficiency, inherited defects of pyruvate dehydrogenase and diabetes.
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Copyright (c) 1996 Acta Neurobiologiae Experimentalis
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