Amyloid‐β (Aβ) dysmetabolism is tightly associated with pathological processes in Alzheimer's disease (AD). Currently, it is thought that, in addition to Aβ fibrils that give rise to plaque formation, Aβ aggregates into non‐fibrillar soluble oligomers (AβOs). Soluble AβOs have been extensively studied for their synaptotoxic and neurotoxic properties. In this review, we discuss physicochemical properties of AβOs and their impact on different brain cell types in AD. Additionally, we summarize three decades of studies with AβOs, providing a compelling bulk of evidence regarding cell‐specific mechanisms of toxicity. Cellular models may lead us to a deeper understanding of the detrimental effects of AβOs in neurons and glial cells, putatively shedding light on the development of innovative therapies for AD.

中文翻译：

---

阿尔茨海默氏病细胞模型中的淀粉样β寡聚体。

淀粉样β（Aβ）代谢异常与阿尔茨海默氏病（AD）的病理过程密切相关。当前，据认为，除了引起斑块形成的Aβ原纤维外，Aβ还聚集成非原纤维可溶性低聚物（AβOs）。可溶性AβOs的突触毒性和神经毒性特性已被广泛研究。在这篇综述中，我们讨论了AβOs的理化性质及其对AD中不同脑细胞类型的影响。此外，我们总结了AβOs的三十年研究，提供了有关细胞特异性毒性机制的大量证据。细胞模型可能使我们对神经元和神经胶质细胞中AβOs的有害作用有更深入的了解，从而为AD的创新疗法的发展提供了可能。