Background:The aberrant accumulation of amyloid-beta (Aβ) in the neocortex and hippocampus is one of the initial causes of Alzheimer's disease (AD). The p75 neurotrophin receptor (p75NTR) has been proposed to mediate Aβ-induced neuronal cell death. Whether p75NTR is required for the effects of Aβ on neuronal network activity,remains unclear. Results: Our results show that low concentrations of Aβ42 did not affect neuronal viability and synapse number. However, the Aβ42 treatment decreased the neuronal network activity of cultured wild-type hippocampal neurons, including a significant decrease of Ca2+ oscillations, spontaneous postsynaptic activity and synaptic connectivity. Moreover, the Aβ42 treatment did not affect the neuronal network activity of Tg2576/p75NTR+/− and p75NTR+/− hippocampal neurons. Conclusion: These studies will shed new light on the pathogenesis of AD and aid the development of related drugs.
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