IMR Press / FBL / Volume 12 / Issue 13 / DOI: 10.2741/2445

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Article

Beta-amyloid peptide – nicotinic acetylcholine receptor interaction: the two faces of health and disease 

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1 Department of Neurology, George and Cynthia Mitchell Research Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX 77555-0874, USA
Front. Biosci. (Landmark Ed) 2007, 12(13), 5030–5038; https://doi.org/10.2741/2445
Published: 1 September 2007
Abstract

Elevated amyloid-beta peptide (Abeta) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery of an Abeta-nAChR interaction, much effort has been expended to understand how this interaction may contribute to normal physiological processes as well as AD. Several researchers have expanded on the initial observation of an Abeta-nAChR interaction to characterize the pertinent factors that confer Abeta sensitivity to nAChRs. Some of which include the following: 1. receptor subunit composition; 2. receptor subunit stoichiometry; 3. regional distribution; 4. presynaptic versus somatic distribution; 5. neuron versus glia expression; 6. in vitro expression system. These aspects of nAChR composition and expression appear to confer the specific functional consequences of Abeta interaction which range from blockade of receptor activation to stimulation of second messenger cascades that provide neuroprotection from Abeta toxicity. This review will discuss the extant literature on the subject in terms of clarifying this apparent dichotomy regarding the consequences of Abeta – nAChR interaction during health and disease.

Keywords
Nicotinic
Cholinergic
Amyloid
Alzheimer's Disease
Neuroprotection
Alpha7
Review
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