Brain plasticity is widely accepted as the core neurophysiological basis of memory and is generally defined by activity-dependent changes in synaptic efficacy, such as long-term potentiation (LTP) and long-term depression (LTD). By using diverse induction protocols like high-frequency stimulation (HFS) or spike-timing dependent plasticity (STDP), such crucial cognition-relevant plastic processes are shown to be impaired in Alzheimer’s disease (AD). In AD, the severity of the cognitive impairment also correlates with the level of disruption of neuronal network dynamics. Currently under debate, the named amyloid hypothesis points to amyloid-beta peptide 1-42 (Aβ42) as the trigger of the functional deviations underlying cognitive impairment in AD. However, there are missing functional mechanistic data that comprehensively dissect the early subtle changes that lead to synaptic dysfunction and subsequent neuronal network collapse in AD. The convergence of the study of both, mechanisms underlying brain plasticity, and neuronal network dynamics, may represent the most efficient approach to address the early triggering and aberrant mechanisms underlying the progressive clinical cognitive impairment in AD. Here we comment on the emerging integrative roles of brain plasticity and network oscillations in AD research and on the future perspectives of research in this field.

中文翻译：

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阿尔茨海默氏病的突触可塑性和振动：多方面疾病的复杂图景。文章类型：透视图

脑可塑性被广泛接受为记忆的核心神经生理基础，并且通常由突触功效的活动依赖性变化来定义，例如长期增强（LTP）和长期抑郁（LTD）。通过使用多种诱导方案，例如高频刺激（HFS）或峰值刺激依赖的可塑性（STDP），这些与认知相关的重要塑性过程被证明在阿尔茨海默氏病（AD）中受损。在AD中，认知障碍的严重程度还与神经元网络动力学的破坏水平相关。目前正在辩论中，命名的淀粉样蛋白假说指出淀粉样蛋白-β肽1-42（Aβ42）是AD认知障碍背后功能偏离的触发因素。然而，缺少完整的解剖早期导致关节突触功能障碍和随后的神经元网络崩溃的细微变化的功能性机械数据。大脑可塑性和神经网络动态机制的研究的融合可能是解决AD中渐进性临床认知障碍基础的早期触发和异常机制的最有效方法。在这里，我们评论了大脑可塑性和网络振荡在AD研究中新兴的整合作用以及该领域研究的未来前景。可能代表解决AD中进行性临床认知障碍的早期触发和异常机制的最有效方法。在这里，我们评论了大脑可塑性和网络振荡在AD研究中新兴的整合作用以及该领域研究的未来前景。可能代表解决AD中进行性临床认知障碍的早期触发和异常机制的最有效方法。在这里，我们评论了大脑可塑性和网络振荡在AD研究中新兴的整合作用以及该领域研究的未来前景。