This review provides a comprehensive examination of the role of clathrin-mediated endocytosis (CME) in Alzheimer’s disease (AD) pathogenesis, emphasizing its impact across various cellular contexts beyond neuronal dysfunction. In neurons, dysregulated CME contributes to synaptic dysfunction, amyloid beta (Aβ) processing, and Tau pathology, highlighting its involvement in early AD pathogenesis. Furthermore, CME alterations extend to non-neuronal cell types, including astrocytes and microglia, which play crucial roles in Aβ clearance and neuroinflammation. Dysregulated CME in these cells underscores its broader implications in AD pathophysiology. Despite significant progress, further research is needed to elucidate the precise mechanisms underlying CME dysregulation in AD and its therapeutic implications. Overall, understanding the complex interplay between CME and AD across diverse cell types holds promise for identifying novel therapeutic targets and interventions.

中文翻译：

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网格蛋白介导的阿尔茨海默氏病内吞作用：细胞类型特异性参与淀粉样蛋白病理学

这篇综述对网格蛋白介导的内吞作用 (CME) 在阿尔茨海默病 (AD) 发病机制中的作用进行了全面检查，强调了其对神经元功能障碍之外的各种细胞环境的影响。在神经元中，失调的 CME 会导致突触功能障碍、β 淀粉样蛋白 (Aβ) 加工和 Tau 病理学，突出显示其参与早期 AD 发病机制。此外，CME 改变延伸至非神经元细胞类型，包括星形胶质细胞和小胶质细胞，它们在 Aβ 清除和神经炎症中发挥着至关重要的作用。这些细胞中 CME 失调强调了其在 AD 病理生理学中更广泛的影响。尽管取得了重大进展，但仍需要进一步研究来阐明 AD 中 CME 失调的确切机制及其治疗意义。总体而言，了解不同细胞类型的 CME 和 AD 之间复杂的相互作用有望确定新的治疗靶点和干预措施。