α7-nicotinic acetylcholine receptors: New therapeutic avenues in alzheimer’s disease

Murat Oz, Georg Petroianu, Dietrich E. Lorke

Research output: Chapter in Book/Report/Conference proceedingChapter

7 Citations (Scopus)

Abstract

Amyloid plaques, derived from aggregates of amyloid β (Aβ), are closely linked to the pathogenesis of Alzheimer’s disease (AD). Another neuropathological hallmark is the loss of cholinergic markers, associated with a reduction in the α7 subunit of the nicotinic acetylcholine receptor (nAChR) in the brains of AD patients. The α7-nAChR plays an important role in circuits involved in learning and memory, and may be a promising target for the treatment of AD. Numerous studies indicate that binding to α7-nAChRs is neuroprotective. However, Aβ has also been shown to induce tau phosphorylation via α7-nAChR activation. In addition, picomolar to nanomolar concentrations of Aβ stimulate presynaptic α7-nAChRs, evoking an increase in presynaptic Ca2+ levels. There is evidence that Aβ infl uences hippocampus-dependent cognitive functions and synaptic plasticity such as long-term potentiation by modulating the function of α7-nAChRs. In line with the roles of α7-nAChRs in AD pathogenesis, allosteric modulators of α7-nAChRs have been proposed as novel therapeutical agents in the treatment of this disease.

Original languageEnglish
Title of host publicationNeuromethods
PublisherHumana Press Inc.
Pages149-169
Number of pages21
Volume117
DOIs
Publication statusPublished - 2016
Externally publishedYes

Publication series

NameNeuromethods
Volume117
ISSN (Print)08932336
ISSN (Electronic)19406045

Keywords

  • Acetylcholinesterase
  • Alzheimer’s disease
  • Amyloid
  • Cholinergic
  • Hippocampus
  • Neuroprotection
  • Nicotinic acetylcholine receptor
  • Review
  • Tau phosphorylation
  • α-Bungarotoxin

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Psychiatry and Mental health

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