综述:星形胶质细胞介导的β-淀粉样蛋白代谢与阿尔茨海默病早期的关系
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国家自然科学基金(30900430, 30970932),教育部留学回国人员科研启动基金([2010]1561号),浙江省自然科学基金(LY12H09001),宁波市自然科学基金(2011A610065, 2009A610128),宁波市创新团队项目(2009B21002),宁波大学学科项目(XKL11D2114)和宁波大学王宽诚幸福基金资助项目


Review:The Relationship Between Astrocyte-mediated Metabolism of β-Amyloid Protein and Pathogenesis of The Early Stages of Alzheimer′s Disease
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This work was supported by grants from The National Natural Science Foundation of China(30900430, 30970932), Scientific Research Foundation for the Returned Overseas Chinese Scholars, The Project-sponsored by SRF for ROCS, SEM ([2010]1561), Zhejiang Provincial Natural Science Foundation (LY12H09001), Ningbo Natural Science Foundation (2011A610065, 2009A610128), Innovative Research Team of Educational Commission of Ningbo(2009B21002), Disciplinary Project of Ningbo University (XKL11D2114) and K.C.Wong Magna Fund in Ningbo University

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    摘要:

    星形胶质细胞是中枢神经系统中含量最丰富的细胞,研究表明,星形胶质细胞与阿尔茨海默病(Alzheimer's disease,AD)病程有关,尤其是对AD主要致病蛋白β-淀粉样蛋白(β-amyloid protein,Aβ)的产生、内化和降解过程起着重要的调节作用.本文讨论星形胶质细胞中Aβ的产生,星形胶质细胞对Aβ的内化、降解和清除的机制,并阐释星形胶质细胞在Aβ代谢中的作用与AD早期发病机制的关系.

    Abstract:

    Alzheimer′s disease(AD), which is characterized with acquired deterioration of cognitive functioning and neuronal loss, is the most common neurodegenerative disease in the elderly population. However, the pathogenesis of AD is still unclear. The accumulation of β-amyloid protein(Aβ) in the brains has been associated with pathogenesis of AD. Studies have shown that astrocytes, the most abundant cells in the central nervous system (CNS), play an important role in the cause and progression of AD by regulating the metabolism of Aβ. The present paper reviews the production, internalization and degradation of Aβ in astrocytes. Our goal is to provide updated views of the role and mechanism of astrocytes in the metabolism of Aβ and its role in pathogenesis in the early stages of Alzheimer′s disease.

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林律,徐淑君,王钦文.综述:星形胶质细胞介导的β-淀粉样蛋白代谢与阿尔茨海默病早期的关系[J].生物化学与生物物理进展,2012,39(8):715-720

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  • 收稿日期:2012-03-17
  • 最后修改日期:2012-06-21
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  • 在线发布日期: 2012-08-21
  • 出版日期: 2012-08-20