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Polymorphisms of chemokine and chemokine receptor genes in Alzheimer's and Parkinson's Patients

机译:阿尔茨海默氏症和帕金森患者中趋化因子和趋化因子受体基因的多态性

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Introduction Several unrelated pathological, genetic, and epidemiological studies have provided an insight into the inflammatory mechanisms involved in the pathogenesis of Alzeimer and Parkinson Disease. The inflammatory process is driven by activated microglia/ astrocytes and by proinflammatory molecules and related signaling pathways, which lead to further inflammatory cell activation. This cascade is mediated by pro-inflammatory cytokines and chemokines such as IL1, IL6, TNF alpha , MIP-1, MCP-1 and RANTES, which set up a noxious network for the neuron survival (1-3). Based on these findings, the major risk of developing the chronic process of degeneration in the brain may be influenced by genetic aspects i.e. the gene polymorphisms of inflammatory agents secreted by activated microglia/astrocyte cells in the nervous tissue and activated monocytes in the blood stream (4).
机译:引言几种无关的病理学,遗传和流行病学研究已经介绍了患有Alzeimer和帕金森病发病机制的炎症机制。炎症过程由活化的微胶质细胞和前炎分子和相关信号传导途径驱动,导致进一步的炎症细胞活化。该级联由促炎细胞因子和趋化因子介导,例如IL1,IL6,TNFα,MIP-1,MCP-1和RANTES,其为神经元存活(1-3)建立了一种有害网络。基于这些发现,发育大脑中变性慢性过程的主要风险可能受到遗传方面的影响,即通过神经组织中激活的微胶质细胞分泌的炎性剂的基因多态性,并在血流中活化单核细胞( 4)。

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