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Perisynaptic accumulations of amyloid β-protein (Aβ) play a critical role in the synaptic dysfunction underlying the cognitive impairment observed in Alzheimer’s disease. The methionine residue at position 35 (Met35) in Aβ is highly subject to oxidation in Alzheimer’s disease brains. In hippocampal brain slices we found that long-term potentiation at CA3–CA1 synapses was significantly inhibited by...
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