Nicotinic acetylcholine receptor interaction with β-amyloid: molecular, cellular, and physiological consequences

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Elevated amyloid-β peptide (Aβ) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's 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.


Original languageEnglish
Pages (from-to)27-39
Number of pages13
JournalCurrent Alzheimer Research
Issue number1
Publication statusPublished - Feb 2010


  • Alzheimer disease, amyloid beta-peptides, animals, humans, nicotinic receptors, signal transduction, nicotinic, cholinergic, amyloid, Alzheimer's disease, neuroprotection

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