Amelioration of amyloid-β-induced deficits by DcR3 in an Alzheimer’s disease model
作者: Yi-Ling LiuWei-Ting ChenYu-Yi LinPo-Hung LuShie-Liang HsiehIrene Han-Juo Cheng
作者单位: 1National Yang-Ming University
2Genomics Research Center, Academia Sinica
3Department of Medical Research and Education, Taipei Veterans General Hospital
刊名: Molecular Neurodegeneration, 2017, Vol.12 (1)
来源数据库: Springer Journal
DOI: 10.1186/s13024-017-0173-0
关键词: Alzheimer's DiseaseNeuroinflammationDecoy Receptor 3M2a microglia
英文摘要: Microglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer’s disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage differentiation toward the M2 anti-inflammatory phenotype. Based on its role as an immunosupressor, we examined whether DcR3 could alleviate neuroinflammation and AD-like deficits in the central nervous system.
原始语种摘要: Microglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer’s disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage differentiation toward the M2 anti-inflammatory phenotype. Based on its role as an immunosupressor, we examined whether DcR3 could alleviate neuroinflammation and AD-like deficits in the central nervous system.
全文获取路径: Springer  (合作)
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来源刊物:
影响因子:4.007 (2012)

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关键词翻译
关键词翻译
  • induced 感应的
  • amyloid 淀粉状朊
  • pleiotropic 多向性的
  • microglia 小神经胶质细胞
  • mediate 
  • pathogenesis 发病机理
  • inflammatory 激怒的
  • macrophage 巨噬细胞
  • receptor 接受体
  • whether 是否