Molecular mechanism of cholinergic dysfunction and cognitive deficits induced by amyloid β-peptide

M. H. Tran, K. Yamada, Toshitaka Nabeshima

Research output: Contribution to journalShort survey

2 Citations (Scopus)

Abstract

Amyloid β-peptide (Aβ) plays a critical role in the development of Alzheimer's disease (AD). Much progress has been made in understanding this age-related neurodegenerative disorder; thus an insight into the cellular actions of Aβ and resulting functional consequences may contribute to preventive and therapeutic approaches for AD. In this review, recent evidence of Aβ-induced brain dysfunction, especially cholinergic impairment and memory deficits, is summarized. Moreover, proposed mechanisms for Aβ-induced neurotoxicity such as oxidative stress, ion-channel formation, and Aβ-receptor interaction are discussed.

Original languageEnglish
Pages (from-to)125-132
Number of pages8
JournalJapanese Journal of Psychopharmacology
Volume21
Issue number4
Publication statusPublished - 29-12-2001

Fingerprint

Amyloid
Cholinergic Agents
Alzheimer Disease
Peptides
Memory Disorders
Ion Channels
Neurodegenerative Diseases
Oxidative Stress
Brain
Cognitive Dysfunction
Therapeutics
peptide A

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

@article{d13b0a5027514dc68cd61d46aaed766d,
title = "Molecular mechanism of cholinergic dysfunction and cognitive deficits induced by amyloid β-peptide",
abstract = "Amyloid β-peptide (Aβ) plays a critical role in the development of Alzheimer's disease (AD). Much progress has been made in understanding this age-related neurodegenerative disorder; thus an insight into the cellular actions of Aβ and resulting functional consequences may contribute to preventive and therapeutic approaches for AD. In this review, recent evidence of Aβ-induced brain dysfunction, especially cholinergic impairment and memory deficits, is summarized. Moreover, proposed mechanisms for Aβ-induced neurotoxicity such as oxidative stress, ion-channel formation, and Aβ-receptor interaction are discussed.",
author = "Tran, {M. H.} and K. Yamada and Toshitaka Nabeshima",
year = "2001",
month = "12",
day = "29",
language = "English",
volume = "21",
pages = "125--132",
journal = "Neuropsychopharmacology Reports",
issn = "1340-2544",
publisher = "John Wiley and Sons Inc.",
number = "4",

}

Molecular mechanism of cholinergic dysfunction and cognitive deficits induced by amyloid β-peptide. / Tran, M. H.; Yamada, K.; Nabeshima, Toshitaka.

In: Japanese Journal of Psychopharmacology, Vol. 21, No. 4, 29.12.2001, p. 125-132.

Research output: Contribution to journalShort survey

TY - JOUR

T1 - Molecular mechanism of cholinergic dysfunction and cognitive deficits induced by amyloid β-peptide

AU - Tran, M. H.

AU - Yamada, K.

AU - Nabeshima, Toshitaka

PY - 2001/12/29

Y1 - 2001/12/29

N2 - Amyloid β-peptide (Aβ) plays a critical role in the development of Alzheimer's disease (AD). Much progress has been made in understanding this age-related neurodegenerative disorder; thus an insight into the cellular actions of Aβ and resulting functional consequences may contribute to preventive and therapeutic approaches for AD. In this review, recent evidence of Aβ-induced brain dysfunction, especially cholinergic impairment and memory deficits, is summarized. Moreover, proposed mechanisms for Aβ-induced neurotoxicity such as oxidative stress, ion-channel formation, and Aβ-receptor interaction are discussed.

AB - Amyloid β-peptide (Aβ) plays a critical role in the development of Alzheimer's disease (AD). Much progress has been made in understanding this age-related neurodegenerative disorder; thus an insight into the cellular actions of Aβ and resulting functional consequences may contribute to preventive and therapeutic approaches for AD. In this review, recent evidence of Aβ-induced brain dysfunction, especially cholinergic impairment and memory deficits, is summarized. Moreover, proposed mechanisms for Aβ-induced neurotoxicity such as oxidative stress, ion-channel formation, and Aβ-receptor interaction are discussed.

UR - http://www.scopus.com/inward/record.url?scp=0035210567&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035210567&partnerID=8YFLogxK

M3 - Short survey

VL - 21

SP - 125

EP - 132

JO - Neuropsychopharmacology Reports

JF - Neuropsychopharmacology Reports

SN - 1340-2544

IS - 4

ER -