TY - JOUR
T1 - Amyloid β-peptide induces cholinergic dysfunction and cognitive deficits
T2 - A minireview
AU - Tran, Manh Hung
AU - Yamada, Kiyofumi
AU - Nabeshima, Toshitaka
N1 - Funding Information:
This study was supported in part by grants-in-aid for Science Research (number 99187 and 12210075), a COE Grant and Special Coordination Funds for the Promotion of Science and Technology, Target-oriented Brain Science Research Program from the Ministry of Education, Culture, Sports, Science and Technology of Japan, and an SRF Grant for Biomedical Research.
PY - 2002
Y1 - 2002
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, particularly of 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, particularly of 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.
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U2 - 10.1016/S0196-9781(02)00062-1
DO - 10.1016/S0196-9781(02)00062-1
M3 - Review article
C2 - 12128084
AN - SCOPUS:0036075848
SN - 0196-9781
VL - 23
SP - 1271
EP - 1283
JO - Peptides
JF - Peptides
IS - 7
ER -