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Current Alzheimer Research

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Nicotinic Acetylcholine Receptor Interaction with β -Amyloid: Molecular, Cellular, and Physiological Consequences

Author(s): H. R. Parri and K. T. Dineley

Volume 7 , Issue 1 , 2010

Page: [27 - 39] Pages: 13

DOI: 10.2174/156720510790274464

Price: $65

Abstract

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

Keywords: Nicotinic, cholinergic, amyloid, Alzheimer's disease, neuroprotection, α7, review


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