Abstract
We previously demonstrated that the growth hormone (GH)-releaser diet ameliorated beta-amyloid (A beta) (1-42)-induced memory impairment, but the underlying mechanism remained to be characterized. We show here that the GH-releaser diet significantly attenuated A beta(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 A beta(1-42)-induced cognitive deficits via stimulation of the hippocampal IGF-1 receptor.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylcholine / metabolism
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Acetylcholinesterase / genetics
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Acetylcholinesterase / metabolism
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Amyloid beta-Peptides / administration & dosage
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Amyloid beta-Peptides / toxicity*
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Animals
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Choline O-Acetyltransferase / genetics
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Choline O-Acetyltransferase / metabolism
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Cognition Disorders / chemically induced
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Cognition Disorders / diet therapy
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Cognition Disorders / prevention & control*
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Diet*
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Growth Hormone / blood
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Growth Hormone / metabolism*
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Hippocampus / drug effects
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Hippocampus / metabolism
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Insulin-Like Growth Factor I / genetics
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Insulin-Like Growth Factor I / metabolism
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Male
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Mice
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Mice, Inbred C57BL
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Peptide Fragments / administration & dosage
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Peptide Fragments / toxicity*
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Receptor, IGF Type 1 / genetics
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Receptor, IGF Type 1 / metabolism
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Receptor, IGF Type 1 / physiology*
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Reverse Transcriptase Polymerase Chain Reaction
Substances
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Amyloid beta-Peptides
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Peptide Fragments
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amyloid beta-protein (1-42)
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Insulin-Like Growth Factor I
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Growth Hormone
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Choline O-Acetyltransferase
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Receptor, IGF Type 1
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Acetylcholinesterase
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Acetylcholine