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Accumulation of amyloid beta (Aβ) protein is a key pathogenic element of Alzheimers disease.It is reported that the Aβ-induced impairments in synaptic plasticity (LTP and LTD) coincides with memory decline and dementia.Although Aβ-induced inhibition of hippocampal long-term potentiation (LTP) has been intensively investigated,the underlying mechanism of Aβ-enhanced long-term depression (LTD) is not clear.