Aβ1-42 inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

被引：279

作者：

Jo, Jihoon ^{[1
]}

Whitcomb, Daniel J. ^{[1
]}

Olsen, Kimberly Moore ^{[2
]}

Kerrigan, Talitha L. ^{[1
]}

Lo, Shih-Ching ^{[2
]}

Bru-Mercier, Gilles ^{[1
]}

Dickinson, Bryony ^{[1
]}

Scullion, Sarah ^{[1
,3
]}

Sheng, Morgan ^{[2
]}

Collingridge, Graham ^{[3
,4
]}

Cho, Kwangwook ^{[1
,3
]}

机构：

[1] Univ Bristol, Sch Clin Sci, Fac Med & Dent, Henry Wellcome Labs Integrat Neurosci & Endocrino, Bristol, Avon, England

[2] Genentech Inc, Dept Neurosci, San Francisco, CA 94080 USA

[3] Univ Bristol, MRC Ctr Synapt Plast, Bristol, Avon, England

[4] Univ Bristol, Sch Physiol & Pharmacol, Bristol, Avon, England

来源：

NATURE NEUROSCIENCE | 2011年 / 14卷 / 05期

基金：

英国生物技术与生命科学研究理事会; 英国医学研究理事会;

关键词：

LONG-TERM POTENTIATION; ALZHEIMERS-DISEASE; SYNAPTIC PLASTICITY; PROTEIN-KINASE; BETA; ACTIVATION; DEPRESSION; OLIGOMERS; MEMORY;

D O I：

10.1038/nn.2785

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

Amyloid-beta(1-42) (A beta) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of A. to inhibit hippocampal long-term potentiation provides a cellular correlate of this action, but the underlying molecular mechanism is only partially understood. We found that a signaling pathway involving caspase-3, Akt1 and glycogen synthase kinase-3b is an important mediator of this effect in rats and mice.

引用

页码：545 / 547

页数：3

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