Aβ1-42 inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β

Amyloid-beta(1-42) (A beta) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of A. 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-3b is an important mediator of this effect in rats and mice.