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
Current Alzheimer Research
Title: Nicotinic Acetylcholine Receptor Interaction with β -Amyloid: Molecular, Cellular, and Physiological Consequences
Volume: 7 Issue: 1
Author(s): H. R. Parri and K. T. Dineley
Affiliation:
Keywords: Nicotinic, cholinergic, amyloid, Alzheimer's disease, neuroprotection, α7, review
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.
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Cite this article as:
Parri R. H. and Dineley T. K., Nicotinic Acetylcholine Receptor Interaction with β -Amyloid: Molecular, Cellular, and Physiological Consequences, Current Alzheimer Research 2010; 7 (1) . https://dx.doi.org/10.2174/156720510790274464
DOI https://dx.doi.org/10.2174/156720510790274464 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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