Abstract
Amyloid-β(1-42) (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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amyloid beta-Peptides / pharmacology*
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Animals
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Animals, Newborn
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Biophysics
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Caspase 3 / deficiency
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Caspase 3 / metabolism*
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Electric Stimulation / methods
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Enzyme Inhibitors / pharmacology
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Glycogen Synthase Kinase 3 / genetics
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Glycogen Synthase Kinase 3 / metabolism*
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Glycogen Synthase Kinase 3 beta
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Green Fluorescent Proteins / genetics
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Hippocampus / cytology
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Hippocampus / drug effects
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Hippocampus / physiology
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Long-Term Potentiation / drug effects*
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Long-Term Potentiation / genetics
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Mice
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Mice, Knockout
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Neurons / drug effects
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Neurons / metabolism
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Organ Culture Techniques
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Patch-Clamp Techniques
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Peptide Fragments / pharmacology*
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism*
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Pyridines / pharmacology
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Pyrimidines / pharmacology
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Rats
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Rats, Wistar
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Signal Transduction / drug effects*
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Signal Transduction / genetics
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Signal Transduction / physiology
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Transfection / methods
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X-Linked Inhibitor of Apoptosis Protein / genetics
Substances
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Amyloid beta-Peptides
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Chir 99021
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Enzyme Inhibitors
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Peptide Fragments
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Pyridines
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Pyrimidines
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X-Linked Inhibitor of Apoptosis Protein
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amyloid beta-protein (1-42)
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Green Fluorescent Proteins
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Akt1 protein, mouse
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Glycogen Synthase Kinase 3 beta
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Gsk3b protein, mouse
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Gsk3b protein, rat
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Proto-Oncogene Proteins c-akt
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Glycogen Synthase Kinase 3
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Caspase 3