摘要

Elevated amyloid-beta peptide (A beta) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery of an A beta - nAChR interaction, much effort has been expended to characterize the consequences of high versus low concentrations of A beta on nAChRs. This review will discuss current knowledge on the subject at the molecular, cellular, and physiological levels with particular emphasis on understanding how A beta - nAChR interaction may contribute to normal physiological processes as well as the etiology of AD.

  • 出版日期2010-2