The Amyloid theory of Alzheimer’s disease (AD) suggests that the deposition of Amyloid β (Aβ) in the brain triggers a chain of events, involving the deposition of phosphorylated Tau and other misfolded proteins, leading to neurodegeneration via neuroinflammation, oxidative stress, and neurovascular factors. The infectious theory linked various infectious agents with the development of AD, raising the possibility that they serve as etiological causes of the disease. Are these theories mutually exclusive, or do they coincide? In this review, we will discuss how the two theories converge. We present a model by which (1) the systemic infectious burden accelerates the development of AD brain pathology via bacterial Amyloids and other pathogen-associated molecular patterns (PAMPs), and (2) the developing AD brain pathology increases its susceptibility to the neurotoxicity of infectious agents -derived PAMPs, which drive neurodegeneration via activated microglia. The reciprocal effects of amyloid deposition and systemic infectious burden may lead to a vicious cycle fueling Alzheimer’s disease pathogenesis.

中文翻译：

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当传染环境遇上AD大脑

阿尔茨海默病 (AD) 的淀粉样蛋白理论表明，β 淀粉样蛋白 (Aβ) 在大脑中的沉积引发一系列事件，包括磷酸化 Tau 和其他错误折叠蛋白的沉积，通过神经炎症、氧化应激和神经血管导致神经变性因素。传染性理论将各种传染性病原体与 AD 的发展联系起来，提高了它们作为疾病病因的可能性。这些理论是相互排斥的，还是一致的？在这篇评论中，我们将讨论这两种理论是如何融合的。我们提出了一个模型，通过该模型 (1) 全身感染负担通过细菌淀粉样蛋白和其他病原体相关分子模式 (PAMP) 加速 AD 脑病理学的发展，(2) 发展中的 AD 脑病理学增加了其对感染因子衍生的 PAMP 的神经毒性的敏感性，这些 PAMP 通过活化的小胶质细胞驱动神经退行性变。淀粉样蛋白沉积和全身感染负担的相互影响可能导致恶性循环，助长阿尔茨海默病的发病机制。