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

Harri R. Parri, T.K. Dineley

Research output: Contribution to journalArticle

Abstract

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.

LanguageEnglish
Pages27-39
Number of pages13
JournalCurrent Alzheimer Research
Volume7
Issue number1
DOIs
Publication statusPublished - Feb 2010

Fingerprint

Amyloid beta-Peptides
Nicotinic Receptors
Amyloid
Alzheimer Disease
Physiological Phenomena

Keywords

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

Cite this

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Nicotinic acetylcholine receptor interaction with β-amyloid : molecular, cellular, and physiological consequences. / R. Parri, Harri; Dineley, T.K.

In: Current Alzheimer Research, Vol. 7, No. 1, 02.2010, p. 27-39.

Research output: Contribution to journalArticle

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