Soluble amyloid-beta oligomers (Aβo) start to accumulate in the human brain one to two decades before any clinical symptoms of Alzheimer's disease (AD) and are implicated in synapse loss, one of the best predictors of memory decline that characterize the illness. Cognitive impairment in AD was traditionally thought to result from a reduction in synaptic activity which ultimately induces neurodegeneration. More recent evidence indicates that in the early stages of AD synaptic failure is, at least partly, induced by neuronal hyperactivity rather than hypoactivity. Here, we review the growing body of evidence supporting the implication of soluble Aβo on the induction of neuronal hyperactivity in AD animal models, in vitro, and in humans. We then discuss the impact of Aβo-induced hyperactivity on memory performance, cell death, epileptiform activity, gamma oscillations, and slow wave activity. We provide an overview of the cellular and molecular mechanisms that are emerging to explain how Aβo induce neuronal hyperactivity. We conclude by providing an outlook on the impact of hyperactivity for the development of disease-modifying interventions at the onset of AD.

可溶性淀粉样β低聚物（Aβo）在阿尔茨海默氏病（AD）的任何临床症状出现前一到二十年就开始在人脑中蓄积，并且与突触丧失有关，突触丧失是这种疾病的最佳记忆力下降指标之一。传统上认为AD的认知障碍是由于突触活动的减少，最终导致神经变性。最近的证据表明，在AD的早期阶段，突触失败至少部分是由神经元过度活跃而不是过度活跃引起的。在这里，我们回顾了越来越多的证据，这些证据支持可溶性Aβo对AD动物模型中神经元过度活跃的诱导的影响，体外，以及人类。然后，我们讨论了Aβo诱导的过度活跃对记忆性能，细胞死亡，癫痫样活动，伽马振荡和慢波活动的影响。我们概述了正在出现的细胞和分子机制，以解释Aβo如何诱导神经元过度活跃。我们通过提供关于多动症在AD发作时对疾病减轻干预措施发展的影响的展望得出结论。