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首页> 外文期刊>Journal of Molecular Biology >Implications of Microglia in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia
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Implications of Microglia in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia

机译：微胶质细胞患者在肌营养侧刀和额颞痴呆症的影响

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摘要

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are neurodegenerative disorders with clear similarities regarding their clinical, genetic and pathological features. Both are progressive, lethal disorders, with no current curative treatment available. Several genes that correlated with ALS and FTD are implicated in the same molecular pathways. Strikingly, many of these genes are not exclusively expressed in neurons, but also in glial cells, suggesting a multicellular pathogenesis. Moreover, chronic inflammation is a common feature observed in ALS and FTD, indicating an essential role of microglia, the resident immune cells of the central nervous system, in disease development and progression. In this review, we will provide a comprehensive overview of the implications of microglia in ALS and FTD. Specifically, we will focus on the role of impaired phagocytosis and increased inflammatory responses and their impact on microglial function. Several genes associated with the disorders can directly be linked to microglial activation, phagocytosis and neuroinflammation. Other genes associated with the disorders are implicated in biological pathways involved in protein degradation and autophagy. In general such mutations have been shown to cause abnormal protein accumulation and impaired autophagy. These impairments have previously been linked to affect the innate immune system in the central nervous system through inappropriate activation of microglia and neuroinflammation, highlighted in this review. Although it has been well established that microglia play essential roles in neurodegenerative disorders, the precise underlying mechanisms remain to be elucidated. (C) 2019 Published by Elsevier Ltd.
机译：肌营养的外侧硬化症（ALS）和额定仪性痴呆（FTD）是神经变性障碍，具有明确的相似性，其临床，遗传和病理特征。两者都是进步，致命的障碍，没有目前的治疗治疗。与Als和FTD相关的几种基因涉及相同的分子途径。尖锐地，许多这些基因在神经元中不仅仅在神经元中表达，而且在胶质细胞中表达，表明多细胞发病机制。此外，慢性炎症是在ALS和FTD中观察到的常见特征，表明小胶质细胞，中枢神经系统的常规免疫细胞在疾病发展和进展中的基本作用。在本次审查中，我们将全面概述MICRIGLIA在ALS和FTD中的影响。具体而言，我们将重点关注吞噬作用有损的作用和增加的炎症反应及其对微胶囊功能的影响。与疾病相关的几个基因可以直接与小胶质激活，吞噬作用和神经引发炎症相关联。与疾病相关的其他基因涉及蛋白质降解和自噬中的生物途径。通常已经显示出这种突变导致异常蛋白质积累和自噬受损。这些损伤以前已被联系起来影响中枢神经系统的先天免疫系统通过不适当的微胶质和神经炎症的激活，突出显示。虽然已经明确地确定了微胶质细胞在神经退行性障碍中发挥基本作用，但仍有待阐明的精确潜在机制。 （c）2019年由elestvier有限公司发布

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  • 来源
    《Journal of Molecular Biology》 |2019年第9期|共12页
  • 作者

    Haukedal Henriette; Freude Kristine;

  • 作者单位

    Univ Copenhagen Fac Hlth &

    Med Sci Dept Vet &

    Anim Sci Grp Stem Cells &

    Modeling Neurodegenerat;

    Univ Copenhagen Fac Hlth &

    Med Sci Dept Vet &

    Anim Sci Grp Stem Cells &

    Modeling Neurodegenerat;

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  • 正文语种 eng
  • 中图分类 分子生物学;
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