Research update: alpha7 nicotinic acetylcholine receptor mechanisms in Alzheimer's disease

Research output: Contribution to journalArticle

View graph of relations Save citation

Open

Authors

Research units

Abstract

Aberrant amyloid-ß peptide (Aß) 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 Aß is bound to a7 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-Aß 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.

Documents

  • Alpha7 nicotinic acetylcholine receptor mechanisms in Alzheimer's disease

    Rights statement: NOTICE: this is the author’s version of a work that was accepted for publication in Biochemical pharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Parri, HR, Hernandez, CM & Dineley, KT, 'Research update: Alpha7 nicotinic acetylcholine receptor mechanisms in Alzheimer's disease', Biochemical pharmacology, vol 82, no. 8 (2011) DOI http://dx.doi.org/10.1016/j.bcp.2011.06.039

    Accepted author manuscript, 513 KB, PDF-document

Details

Original languageEnglish
Pages (from-to)931-942
Number of pages12
JournalBiochemical Pharmacology
Volume82
Issue number8
Early online date7 Jul 2011
DOIs
Publication statusPublished - 15 Oct 2011

    Keywords

  • allosteric regulation, Alzheimer disease, amyloid beta-peptides, animals binding sites, cognition, humans, learning, memory, protein binding, nicotinic receptors, signal transduction, synaptic transmission

Download statistics

No data available

Employable Graduates; Exploitable Research

Copy the text from this field...