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Nat Neurosci. 2011 May;14(5):545-7. doi: 10.1038/nn.2785. Epub 2011 Mar 27.

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

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1
Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, School of Clinical Sciences, Faculty of Medicine and Dentistry, University of Bristol, Bristol, UK.

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.

PMID:
21441921
DOI:
10.1038/nn.2785
[Indexed for MEDLINE]

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