Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

Jihoon Jo, Daniel J Whitcomb, Kimberly Moore Olsen, Talitha L Kerrigan, Shih-Ching Lo, Gilles Bru-Mercier, Bryony Dickinson, Sarah Scullion, Morgan Sheng, Graham Collingridge, Kei Cho

Research output: Contribution to journalArticle (Academic Journal)peer-review

232 Citations (Scopus)

Abstract

Amyloid-β(1-42) (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of Aβ 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-3β is an important mediator of this effect in rats and mice.
Translated title of the contributionAβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β
Original languageEnglish
Pages (from-to)545 - 547
Number of pages3
JournalNature Neuroscience
Volume14
Issue number5
Early online date27 Mar 2011
DOIs
Publication statusPublished - May 2011

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