Neuronal nicotinic acetylcholine receptors serve as sensitive targets that mediate β-amyloid neurotoxicity

Qiang Liu, Jie Wu

Research output: Contribution to journalReview articlepeer-review

23 Scopus citations

Abstract

Alzheimer's disease (AD) is the most common form of brain dementia characterized by the accumulation of β-amyloid peptides (Aβ) and loss of forebrain cholinergic neurons. Aβ accumulation and aggregation are thought to contribute to cholinergic neuronal degeneration, in turn causing learning and memory deficits, but the specific targets that mediate Aβ neurotoxicity remain elusive. Recently, accumulating lines of evidence have demonstrated that Aβ directly modulates the function of neuronal nicotinic acetylcholine receptors (nAChRs), which leads to the new hypothesis that neuronal nAChRs may serve as important targets that mediate Aβ neurotoxicity. In this review, we summarize current studies performed in our laboratory and in others to address the question of how Aβ modulates neuronal nAChRs, especially nAChR subunit function.

Original languageEnglish (US)
Pages (from-to)1277-1286
Number of pages10
JournalActa Pharmacologica Sinica
Volume27
Issue number10
DOIs
StatePublished - Oct 2006
Externally publishedYes

Keywords

  • β-amyloid peptides
  • Alzheimer's disease
  • Neurodegeneration
  • Nicotinic acetylcholine receptor

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Fingerprint

Dive into the research topics of 'Neuronal nicotinic acetylcholine receptors serve as sensitive targets that mediate β-amyloid neurotoxicity'. Together they form a unique fingerprint.

Cite this