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论文题目: Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases
英文论文题目: Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases
第一作者: Tang, Y; Le, WD
英文第一作者: Tang, Y; Le, WD
联系作者: Le, WD (reprint author), Dalian Med Univ, Affiliated Hosp 1, Ctr Translat Res Neurol Dis, Dalian 116011, Peoples R China.
英文联系作者: Le, WD (reprint author), Dalian Med Univ, Affiliated Hosp 1, Ctr Translat Res Neurol Dis, Dalian 116011, Peoples R China.
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发表年度: 2016
卷: 53
期: 2
页码: 1181-1194
摘要: One of the most striking hallmarks shared by various neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease (AD), and amyotrophic lateral sclerosis, is microglia-mediated neuroinflammation. Increasing evidence indicates that microglial activation in the central nervous system is heterogeneous, which can be categorized into two opposite types: M1 phenotype and M2 phenotype. Depending on the phenotypes activated, microglia can produce either cytotoxic or neuroprotective effects. In this review, we focus on the potential role of M1 and M2 microglia and the dynamic changes of M1/M2 phenotypes that are critically associated with the neurodegenerative diseases. Generally, M1 microglia predominate at the injury site at the end stage of disease, when the immunoresolution and repair process of M2 microglia are dampened. This phenotype transformation is very complicated in AD due to the phagocytosis of regionally distributed beta-amyloid (A beta) plaque and tangles that are released into the extracellular space. The endogenous stimuli including aggregated alpha-synuclein, mutated superoxide dismutase, A beta, and tau oligomers exist in the milieu that may persistently activate M1 pro-inflammatory responses and finally lead to irreversible neuron loss. The changes of microglial phenotypes depend on the disease stages and severity; mastering the stage-specific switching of M1/M2 phenotypes within appropriate time windows may provide better therapeutic benefit.
英文摘要: One of the most striking hallmarks shared by various neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease (AD), and amyotrophic lateral sclerosis, is microglia-mediated neuroinflammation. Increasing evidence indicates that microglial activation in the central nervous system is heterogeneous, which can be categorized into two opposite types: M1 phenotype and M2 phenotype. Depending on the phenotypes activated, microglia can produce either cytotoxic or neuroprotective effects. In this review, we focus on the potential role of M1 and M2 microglia and the dynamic changes of M1/M2 phenotypes that are critically associated with the neurodegenerative diseases. Generally, M1 microglia predominate at the injury site at the end stage of disease, when the immunoresolution and repair process of M2 microglia are dampened. This phenotype transformation is very complicated in AD due to the phagocytosis of regionally distributed beta-amyloid (A beta) plaque and tangles that are released into the extracellular space. The endogenous stimuli including aggregated alpha-synuclein, mutated superoxide dismutase, A beta, and tau oligomers exist in the milieu that may persistently activate M1 pro-inflammatory responses and finally lead to irreversible neuron loss. The changes of microglial phenotypes depend on the disease stages and severity; mastering the stage-specific switching of M1/M2 phenotypes within appropriate time windows may provide better therapeutic benefit.
刊物名称: MOLECULAR NEUROBIOLOGY
英文刊物名称: MOLECULAR NEUROBIOLOGY
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学科: Neurosciences
英文学科: Neurosciences
影响因子: 6.19
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论文类别: Article
英文论文类别: Article
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