The inflammatory process has a fundamental role in the pathogenesis of Alzheimer's disease (AD). Recent studies indicate that inflammation is not merely a bystander in neurodegeneration but a powerful pathogenetic force in the disease process. Increased production of amyloid-beta peptide species can activate the innate immunity system via pattern recognition receptors (PRRs) and evoke Alzheimer's pathology. We will focus on the role of innate immunity system of brain in the initiation and the propagation of inflammatory process in AD. We examine here in detail the significance of amyloid-beta oligomers and fibrils as danger-associated molecular patterns (DAMPs) in the activation of a wide array of PRRs in glial cells and neurons, such as Toll-like, NOD-like, formyl peptide, RAGE and scavenger receptors along with complement and pentraxin systems. We also characterize the signaling pathways triggered by different PRRs in evoking inflammatory responses. In addition, we will discuss whether AD pathology could be the outcome of chronic activation of the innate immunity defence in the brain of AD patients.

中文翻译：

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阿尔茨海默氏病的炎症：β-淀粉样蛋白低聚物通过模式识别受体触发先天免疫防御。

炎症过程在阿尔茨海默氏病（AD）的发病机理中具有基本作用。最近的研究表明，炎症不仅是神经退行性疾病的旁观者，而且是疾病过程中强大的致病力。淀粉样蛋白-β肽类物质产量的增加可以通过模式识别受体（PRR）激活先天免疫系统，并引起阿尔茨海默氏病。我们将集中研究大脑先天免疫系统在AD炎症过程的起始和传播中的作用。我们在这里详细检查淀粉样蛋白-β低聚物和原纤维作为危险相关分子模式（DAMPs）在胶质细胞和神经元中广泛的PRR激活中的重要性，例如Toll样，NOD样，甲酰基肽，RAGE和清除剂受体，以及补体和戊traxin系统。我们还表征了在引发炎症反应中由不同的PRR触发的信号通路。此外，我们将讨论AD病理是否可能是AD患者大脑中先天免疫防御的慢性激活的结果。