Aβ inhibition of LTP is prevented by manipulation of a signalling pathway involving caspase-3, Akt and GSK-3β

Amyloid-β1-42 (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease (AD). The ability of Aβ to inhibit hippocampal long-term potentiation (LTP) provides a cellular correlate of this action but the underlying molecular mechanism is only partially understood. We report a prominent role for a signaling pathway involving caspase-3, Akt1 and glycogen synthase kinase-3β in this effect in rats and mice.