Growth Hormone–Releaser Diet Attenuates β-Amyloid(1-42)–Induced Cognitive Impairment via Stimulation of the Insulin-Like Growth Factor (IGF)-1 Receptor in Mice

Abstract

We previously demonstrated that the growth hormone (GH)-releaser diet ameliorated β-amyloid (Aβ) (1-42)–induced memory impairment, but the underlying mechanism remained to be characterized. We show here that the GH-releaser diet significantly attenuated Aβ(1-42)-induced impairment in context-dependent conditioned fear, with a reduction in GH levels and changes in hippocampal acetylcholine, acetylcholinesterase, choline acetyltransferase, insulin-like growth factor (IGF)-1, and IGF-1–receptor activity in mice. JB-1, an IGF-1–receptor antagonist, significantly blocked GH-releaser diet–mediated pharmacological actions. Our results suggest that the GH-releaser diet prevents Aβ(1-42)-induced cognitive deficits via stimulation of the hippocampal IGF-1 receptor.