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The role of immunity and neuroinflammation in genetic predisposition and pathogenesis of Alzheimer's disease

机译：免疫和神经炎症在阿尔茨海默氏病遗传易感性和发病机制中的作用

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Alzheimer's disease is an important public concern with rising prevalence across the globe. While many therapeutic approaches for Alzheimer's disease have been developed, there are currently no validated disease-modifying treatments. Thus, in order to develop novel treatment strategies, there is a significant need to progress our understanding of the pathogenesis of Alzheimer's disease. Several large genome-wide association studies and whole genome and exome sequencing studies have identified novel genes associated with late-onset Alzheimer's disease. Interestingly, many of the genes are associated with inflammation and the immune system, including complement receptor 1, clusterin, CD33, EPH receptor A1, membrane-spanning 4-domains subfamily A, ATP-binding cassette sub-family A member 7, major histocompatibility complex class II, inositol polyphosphate-5-phosphatase, myocyte enhancer factor 2C, and triggering receptor expressed on myeloid cells 2. The pathogenetic contributions of immune reaction and neuroinflammation in Alzheimer's disease have been regarded largely as part of amyloid cascade hypothesis. The neurotoxic amyloid-β (Aβ) induces activation of immune cells, such as microglia, astrocytes, perivascular macrophages and lymphocytes and decreased capability of clearing Aβ by immune system and chronic inflammation caused by activated immune cells aggravate neuronal damage and eventually Alzheimer's disease. But the precise mechanism and hereditary impact on such process is largely unknown. The current findings in genetic studies suggest that the immunological mechanisms of Alzheimer's disease may extend beyond passive reaction of Aβ, including the development of Alzheimer's disease such as time of onset and rate of progression. In this article, we aimed to review the mechanisms of immune reaction and neuroinflammation in Alzheimer's disease, with an emphasis on the function of genes known to be associated with a risk of Alzheimer's disease in terms of neuroinflammation and immune function.
机译：随着全球患病率的上升，阿尔茨海默氏病成为公众关注的重要问题。尽管已经开发出许多用于治疗阿尔茨海默氏病的方法，但目前尚无经过验证的疾病缓解疗法。因此，为了开发新的治疗策略，非常需要增进我们对阿尔茨海默氏病发病机理的理解。几项大型的全基因组关联研究以及全基因组和外显子组测序研究已经确定了与晚期阿尔茨海默氏病相关的新基因。有趣的是，许多基因与炎症和免疫系统有关，包括补体受体1，簇蛋白，CD33，EPH受体A1，跨膜4结构域亚家族A，ATP结合盒亚家族A成员7，主要组织相容性。复杂的II类，肌醇多磷酸5磷酸酶，肌细胞增强因子2C和在骨髓细胞上表达的触发受体2。在阿尔茨海默氏病中，免疫反应和神经炎症的致病作用在很大程度上被认为是淀粉样蛋白级联假说的一部分。具有神经毒性的β-淀粉样蛋白（Aβ）诱导小胶质细胞，星形胶质细胞，血管周巨噬细胞和淋巴细胞等免疫细胞的活化，以及由免疫系统清除Aβ的能力降低，活化的免疫细胞引起的慢性炎症加剧了神经元损害，最终加剧了阿尔茨海默氏病。但是对这种过程的确切机制和遗传影响在很大程度上尚不清楚。遗传学研究的当前发现表明，阿尔茨海默氏病的免疫学机制可能超出了Aβ的被动反应，包括阿尔茨海默氏病的发展，例如发病时间和进展速度。在本文中，我们旨在回顾阿尔茨海默氏病的免疫反应和神经炎症的机制，重点是就神经炎症和免疫功能而言，已知与阿尔茨海默氏病风险相关的基因的功能。

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