Research update: Alpha7 nicotinic acetylcholine receptor mechanisms in Alzheimer's disease.

Abstract

Aberrant amyloid-β peptide (Aβ) accumulation along with altered expression and function of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery that Aβ is bound to α7 nAChRs under many experimental settings, including post-mortem AD brain, much effort has been expended to understand the implications of this interaction in the disease milieu. This research update will review the current literature on the α7 nAChR-Aβ interaction in vitro and in vivo, the functional consequences of this interaction from sub-cellular to cognitive levels, and discuss the implications these relationships might have for AD therapies.

• Authors: H Rheinallt Parri, Caterina M Hernandez, Kelly T Dineley
• Journal: Biochemical pharmacology (Biochem Pharmacol) Vol. 82 Issue 8 Pg. 931-42 (Oct 15 2011) ISSN: 1873-2968 [Electronic] England
• PMID: 21763291 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2011 Elsevier Inc. All rights reserved.

Chemical References

• Amyloid beta-Peptides
• Chrna7 protein, human
• Receptors, Nicotinic
• alpha7 Nicotinic Acetylcholine Receptor

Topics

• Allosteric Regulation
• Alzheimer Disease (drug therapy, etiology, metabolism, physiopathology)
• Amyloid beta-Peptides (metabolism)
• Animals
• Cognition (physiology)
• Humans
• Learning (physiology)
• Memory (physiology)
• Protein Binding
• Receptors, Nicotinic (metabolism)
• Signal Transduction
• Synaptic Transmission
• alpha7 Nicotinic Acetylcholine Receptor