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

被引：170

作者：

Parri, H. Rheinallt ^{[2
]}

Hernandez, Caterina M. ^{[1
]}

Dineley, Kelly T. ^{[1
]}

机构：

[1] Univ Texas Med Branch, Dept Neurol, Galveston, TX USA

[2] Aston Univ, Sch Life & Hlth Sci, Birmingham B4 7ET, W Midlands, England

来源：

BIOCHEMICAL PHARMACOLOGY | 2011年 / 82卷 / 08期

关键词：

Alzheimer's disease; Cholinergic; Amyloid; Oligomer; Neuroprotection; Review; BETA-AMYLOID PEPTIDE; BUNGAROTOXIN BINDING-SITES; HIPPOCAMPAL SYNAPTIC PLASTICITY; ALLOSTERIC TRANSMEMBRANE SITE; CENTRAL-NERVOUS-SYSTEM; TRANSGENIC MICE; UP-REGULATION; A-BETA; GROWTH-FACTOR; MOUSE MODEL;

D O I：

10.1016/j.bcp.2011.06.039

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Aberrant amyloid-P peptide (A beta) 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 A beta is bound to alpha 7 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 a7 nAChR-A beta 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. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：931 / 942

页数：12

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