Alzheimer's disease (AD) is characterized by memory loss, cognitive decline, and devastating neurodegeneration, not only as a result of the extracellular accumulation of beta-amyloid peptide (Aβ) and intracellular accumulation of tau, but also as a consequence of the dysfunction and loss of synapses. Although significant advances have been made in our understanding of the relationship of the pathological role of Aβ and tau in synapse dysfunction, several questions remain as to how Aβ and tau interdependently cause impairments in synaptic function in AD. Overall, more insight into these questions should enable researchers in this field to develop novel therapeutic targets to mitigate or delay the cognitive deficits associated with this devastating disease.

中文翻译：

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阿尔茨海默病的突触障碍：失调的交响乐

阿尔茨海默病 (AD) 的特点是记忆力减退、认知能力下降和破坏性神经变性，这不仅是由于 β-淀粉样肽 (Aβ) 的细胞外积聚和 tau 的细胞内积聚，而且是功能障碍和突触丢失。尽管我们对 Aβ 和 tau 在突触功能障碍中的病理作用关系的理解取得了重大进展，但关于 Aβ 和 tau 如何相互依赖地导致 AD 突触功能受损的问题仍然存在。总体而言，对这些问题的深入了解将使该领域的研究人员能够开发新的治疗靶点，以减轻或延迟与这种破坏性疾病相关的认知缺陷。