阿尔茨海默症（Alzheimer’s disease，AD）是一种以β-淀粉样蛋白（Amyloid-β，Aβ）沉积、tau蛋白缠结和 神经炎症为主要病理特征的神经退行性疾病。传统观点认为Aβ是AD病理过程中的致病毒性物质，但近年 研究发现Aβ可能是一种古老的天然免疫效应分子，具有抗菌功能。本文综述了学术界近年来在Aβ与脂多 糖（lipopolysaccharide，LPS）的相互作用现象与机制方面的研究进展，探讨了Aβ通过直接抗菌、促进病原体聚 集、免疫调节等多种途径发挥抗感染功能的证据，分析了这些发现对“Aβ抗菌保护假说”的支持，并讨论了通 过调节Aβ水平或靶向感染源来干预AD进程的治疗策略。这些新见解不仅拓展了对AD发病机制的认识， 更为开发创新性治疗手段提供了重要理论依据和潜在干预靶点。

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by pathological hallmarks including β-amyloid（Aβ）deposition, tau protein tangles,and neuroinflammation. The traditional theory proposed that Aβ is a pathogenic substance in the pathological process of AD. However, recent studies have found that Aβ may be an ancient natural immune effector with antibacterial functions. In this review, we summarized the research progress on the interaction phenomena and mechanisms between Aβ and lipopolysaccharide (LPS), including the evidence that Aβ has antimicrobial activity such as direct antibacterial activity, promotion of pathogen aggregation, and immune regulation. We also analyzed the support of these findings for the hypothesis of“Aβ antimicrobial and protection hypothesis”and discussed the therapeutic strategies of regulating Aβ levels or targeting infections. These new insights may expand the understanding of the pathogenesis of AD and provide an important theoretical basis and potential intervention targets for the development of innovative therapeutic methods.