Aβ1–42 inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β
J Jo, DJ Whitcomb, KM Olsen, TL Kerrigan, SC Lo… - Nature …, 2011 - nature.com
J Jo, DJ Whitcomb, KM Olsen, TL Kerrigan, SC Lo, G Bru-Mercier, B Dickinson, S Scullion…
Nature neuroscience, 2011•nature.comAbstract Amyloid-β1–42 (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.
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.
Abstract
Amyloid-β1–42 (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.
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