| Literature DB >> 21441921 |
Jihoon Jo1, Daniel J Whitcomb, Kimberly Moore Olsen, Talitha L Kerrigan, Shih-Ching Lo, Gilles Bru-Mercier, Bryony Dickinson, Sarah Scullion, Morgan Sheng, Graham Collingridge, Kwangwook Cho.
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.Entities:
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Year: 2011 PMID: 21441921 DOI: 10.1038/nn.2785
Source DB: PubMed Journal: Nat Neurosci ISSN: 1097-6256 Impact factor: 24.884