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

H. R. Parri, Kelly Dineley

Research output: Contribution to journalArticle

50 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)27-39
Number of pages13
JournalCurrent Alzheimer Research
Volume7
Issue number1
DOIs
StatePublished - Jan 2010

Fingerprint

Nicotinic Receptors
Amyloid
Alzheimer Disease
Physiological Phenomena
peptide A

Keywords

  • α7
  • Alzheimer's disease
  • Amyloid
  • Cholinergic
  • Neuroprotection
  • Nicotinic
  • Review

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

Nicotinic acetylcholine receptor interaction with β-amyloid : Molecular, cellular, and physiological consequences. / Parri, H. R.; Dineley, Kelly.

In: Current Alzheimer Research, Vol. 7, No. 1, 01.2010, p. 27-39.

Research output: Contribution to journalArticle

@article{13691dde0f484daaaa00a0bc841802b5,
title = "Nicotinic acetylcholine receptor interaction with β-amyloid: Molecular, cellular, and physiological consequences",
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.",
keywords = "α7, Alzheimer's disease, Amyloid, Cholinergic, Neuroprotection, Nicotinic, Review",
author = "Parri, {H. R.} and Kelly Dineley",
year = "2010",
month = "1",
doi = "10.2174/156720510790274464",
language = "English (US)",
volume = "7",
pages = "27--39",
journal = "Current Alzheimer Research",
issn = "1567-2050",
publisher = "Bentham Science Publishers B.V.",
number = "1",

}

TY - JOUR

T1 - Nicotinic acetylcholine receptor interaction with β-amyloid

T2 - Molecular, cellular, and physiological consequences

AU - Parri, H. R.

AU - Dineley, Kelly

PY - 2010/1

Y1 - 2010/1

N2 - 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.

AB - 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.

KW - α7

KW - Alzheimer's disease

KW - Amyloid

KW - Cholinergic

KW - Neuroprotection

KW - Nicotinic

KW - Review

UR - http://www.scopus.com/inward/record.url?scp=77949681543&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77949681543&partnerID=8YFLogxK

U2 - 10.2174/156720510790274464

DO - 10.2174/156720510790274464

M3 - Article

C2 - 20205670

AN - SCOPUS:77949681543

VL - 7

SP - 27

EP - 39

JO - Current Alzheimer Research

JF - Current Alzheimer Research

SN - 1567-2050

IS - 1

ER -