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      Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β.

      Nature neuroscience
      Amyloid beta-Peptides, pharmacology, Animals, Animals, Newborn, Biophysics, Caspase 3, deficiency, metabolism, Electric Stimulation, methods, Enzyme Inhibitors, Glycogen Synthase Kinase 3, genetics, Green Fluorescent Proteins, Hippocampus, cytology, drug effects, physiology, Long-Term Potentiation, Mice, Mice, Knockout, Neurons, Organ Culture Techniques, Patch-Clamp Techniques, Peptide Fragments, Proto-Oncogene Proteins c-akt, Pyridines, Pyrimidines, Rats, Rats, Wistar, Signal Transduction, Transfection, X-Linked Inhibitor of Apoptosis Protein

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          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.

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