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学科主题基础医学
Astrocytes: Implications for Neuroinflammatory Pathogenesis of Alzheimer′s Disease
Li, Chuanyu1,2,3,7; Zhao, Rui1,2,3; Gao, Kai1,2,3; Wei, Zheng1,2,3; Yin, Michael Yaoyao1,2,3; Lau, Lok Ting1,2,3,4,5,7; Chui, Dehua1,2,3; Yu, Albert Cheung Hoi1,2,3,4,5,6,7
关键词Alzheimer&prime s disease astrocyte inflammation cytokine chemokine amyloid beta
刊名CURRENT ALZHEIMER RESEARCH
2011-02-01
8期:1页:67-80
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Clinical Neurology ; Neurosciences
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; AMYLOID PRECURSOR PROTEIN ; CENTRAL-NERVOUS-SYSTEM ; NECROSIS-FACTOR-ALPHA ; GROWTH-FACTOR-BETA ; CEREBROSPINAL-FLUID LEVELS ; MILD COGNITIVE IMPAIRMENT ; CULTURED HUMAN ASTROCYTES ; TEMPORAL-LOBE EPILEPSY ; TRANSGENIC MOUSE MODEL
英文摘要

Alzheimer′s disease (AD) is a neurodegenerative disease with major clinical hallmarks of memory loss, dementia, and cognitive impairment. Neuroinflammation is involved in the onset of several neurodegenerative disorders. Astrocyte is the most abundant type of glial cells in the central nervous system (CNS) and appears to be involved in the induction of neuroinflammation. Under stress and injury, astrocytes become astrogliotic leading to an upregulation of the expression of proinflammatory cytokines and chemokines, which are associated with the pathogenesis of AD. Cytokines and related molecules play roles in both neuroprotection and neurodegeneration in the CNS. During early AD pathogenesis, amyloid beta (A beta), S100B and IL-1 beta could bring about a vicious cycle of A beta generation between astrocytes and neurons leading to chronic, sustained and progressive neuroinflammation. In advanced stages of AD, TRAIL secreted from astrocytes have been shown to bind to death receptor 5 (DR5) on neurons to trigger apoptosis in a caspase-8-dependent manner. Furthermore, astrocytes could be reactivated by TGF beta 1 to generate more A beta and to undergo the aggravating astrogliosis. TGF beta 2 was also observed to cooperate with A beta to cause neuronal demise by destroying the stability of lysosomes in neurons. Inflammatory molecules can be either potential biomarkers for diagnosis or target molecules for therapeutic intervention. Understanding their roles and their relationship with activated astrocytes is particularly important for attenuating neuroinflammation in the early stage of AD. The main purpose of this review is to provide a comprehensive insight into the role of astrocytes in the neuroinflammatory pathogenesis of AD.

语种英语
WOS记录号WOS:000287800900007
项目编号31070974 ; 30270426 ; 30470543 ; 30670644 ; 30870818 ; 7032026 ; 7051004 ; 7091004 ; 2011CB504400 ; 2006AA02Z452
资助机构National Natural Science Foundation of China ; Beijing Natural Science Foundation ; National Basic Research Program of China (973 program) ; National High Technology Research and Development Program of China (863 Program)
引用统计
被引频次:94[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/59510
专题北京大学基础医学院_神经生物学系
北京大学第一临床医学院_急诊科
作者单位1.Peking Univ, Neurosci Res Inst, Dept Neurobiol, Hlth Sci Ctr,Sch Basic Med Sci, Beijing 100191, Peoples R China
2.Peking Univ, Minist Educ, Key Lab Neurosci, Beijing 100191, Peoples R China
3.Peking Univ, Minist Publ Hlth, Key Lab Neurosci, Beijing 100191, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Ctr Infect Dis, Beijing 100191, Peoples R China
5.Hai Kang Life Corp Ltd, Shau Kei Wan, Hong Kong, Peoples R China
6.Peking Univ, Inst Syst Biomed, Lab Translat Med, Beijing 100191, Peoples R China
7.Beijing Hai Kang DNA Chips Ltd, Beijing Econ Dev Area, Beijing, Peoples R China
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GB/T 7714
Li, Chuanyu,Zhao, Rui,Gao, Kai,等. Astrocytes: Implications for Neuroinflammatory Pathogenesis of Alzheimer′s Disease[J]. CURRENT ALZHEIMER RESEARCH,2011,8(1):67-80.
APA Li, Chuanyu.,Zhao, Rui.,Gao, Kai.,Wei, Zheng.,Yin, Michael Yaoyao.,...&Yu, Albert Cheung Hoi.(2011).Astrocytes: Implications for Neuroinflammatory Pathogenesis of Alzheimer′s Disease.CURRENT ALZHEIMER RESEARCH,8(1),67-80.
MLA Li, Chuanyu,et al."Astrocytes: Implications for Neuroinflammatory Pathogenesis of Alzheimer′s Disease".CURRENT ALZHEIMER RESEARCH 8.1(2011):67-80.
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