免疫炎症反应与肌萎缩侧索硬化症
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- 论文作者：张宏伟 ; 张晋霞 ; 张志勇
- 年：2016
- 作者机构：河北省遵化市人民医院神经内科;华北理工大学附属医院神经内科;华北理工大学附属医院神经外科;
- 论文关键词：免疫炎症反应 ; 肌萎缩侧索硬化 ; 发病机制
- 会议召开时间：2016-11-25
- 会议录名称：湖南中医药大学学报2016/专集：国际数字医学会数字中医药分会成立大会暨首届数字中医药学术交流会论文集
- 语种：中文
- 分类号：R744.8
- 学会代码：HNZY
- 会议名称：国际数字医学会数字中医药分会成立大会暨首届数字中医药学术交流会
- 会议地点：中国广东珠海
- 主办单位：国际数字医学会、Digital Chinese Medicine
- 学会名称：湖南中医药大学期刊杂志社
- 页数：1
- 文件大小：1809k
- 原文格式：D
- 会议级别：全国
摘要
肌萎缩侧索硬化(amyotrophic lateral sclerosis,ALS)是一种选择性累及运动系统上下运动神经元的中枢神经系统退行性疾病[1]。目前该病病因及发病机制并不十分清楚。由于缺乏有效的治疗手段,平均生存期仅为3-5年。而阐明该病的病因及发病机制可能有助于对该疾病治疗研究提供进一步重要的线索。
引文
[1]Rowland LP,Shneider NA.Amyotrophic lateral sclerosis.N Engl J Med,2001,344(22):1688-1700.
[2]Philips T,Robberecht W.Neuroinflammation in amyotrophic lateral sclerosis:role of glial activation in motor neuron disease.Lancet Neurol,2011,10(3):253-263.
[3]Mc Combe PA,Henderson RD.The Role of immune and inflammatory mechanisms in ALS.Curr Mol Med,2011,11(3):246-254.
[4]Rentzos M,Evangelopoulos E,Sereti E,et al.Alterations of T cell subsets in ALS:a systemic immune activation?Acta Neurol Scand,2012,125(4):260-264.
[5]Carter JR,Mynlieff M.Amyotrophic lateral sclerosis patient Ig G alters voltage dependence of Ca2+channels in dissociated rat motoneurons.Neurosci Lett,2003,353(3):221-225.
[6]Engelhardt JI,Siklos L,Appel SH.Altered calcium homeostasis and ultrastructure in motoneurons of mice caused by passively transferred anti-motoneuronal Ig G.J Neuropathol Exp Neurol,1997,56(1):21-39.
[7]Engelhardt JI,Soos J,Obal I,et al.Subcellular localization of Ig G from the sera of ALS patients in the nervous system.Acta Neurol Scand,2005,112(2):126-133.
[8]Pullen AH,Demestre M,Howard RS,et al.Passive transfer of purified Ig G from patients with amyotrophic lateral sclerosis to mice results in degeneration of motor neurons accompanied by Ca2+enhancement.Acta Neuropathol,2004,107(1):35-46.
[9]Smith RG,Siklos L,Alexianu ME,et al.Autoimmunity and ALS.Neurology,1996,47(4Suppl 2):S40-45;discussion S45-46.
[10]Woodruff TM,Costantini KJ,Crane JW,et al.The complement factor C5a contributes to pathology in a rat model of amyotrophic lateral sclerosis.J Immunol,2008,181(12):8727-8734.
[11]Beers DR,Henkel JS,Zhao W,et al.CD4+T cells support glial neuroprotection,slow disease progression,and modify glial morphology in an animal model of inherited ALS.Proc Natl Acad Sci U S A,2008,105(40):15558-15563.
[2]Philips T,Robberecht W.Neuroinflammation in amyotrophic lateral sclerosis:role of glial activation in motor neuron disease.Lancet Neurol,2011,10(3):253-263.
[3]Mc Combe PA,Henderson RD.The Role of immune and inflammatory mechanisms in ALS.Curr Mol Med,2011,11(3):246-254.
[4]Rentzos M,Evangelopoulos E,Sereti E,et al.Alterations of T cell subsets in ALS:a systemic immune activation?Acta Neurol Scand,2012,125(4):260-264.
[5]Carter JR,Mynlieff M.Amyotrophic lateral sclerosis patient Ig G alters voltage dependence of Ca2+channels in dissociated rat motoneurons.Neurosci Lett,2003,353(3):221-225.
[6]Engelhardt JI,Siklos L,Appel SH.Altered calcium homeostasis and ultrastructure in motoneurons of mice caused by passively transferred anti-motoneuronal Ig G.J Neuropathol Exp Neurol,1997,56(1):21-39.
[7]Engelhardt JI,Soos J,Obal I,et al.Subcellular localization of Ig G from the sera of ALS patients in the nervous system.Acta Neurol Scand,2005,112(2):126-133.
[8]Pullen AH,Demestre M,Howard RS,et al.Passive transfer of purified Ig G from patients with amyotrophic lateral sclerosis to mice results in degeneration of motor neurons accompanied by Ca2+enhancement.Acta Neuropathol,2004,107(1):35-46.
[9]Smith RG,Siklos L,Alexianu ME,et al.Autoimmunity and ALS.Neurology,1996,47(4Suppl 2):S40-45;discussion S45-46.
[10]Woodruff TM,Costantini KJ,Crane JW,et al.The complement factor C5a contributes to pathology in a rat model of amyotrophic lateral sclerosis.J Immunol,2008,181(12):8727-8734.
[11]Beers DR,Henkel JS,Zhao W,et al.CD4+T cells support glial neuroprotection,slow disease progression,and modify glial morphology in an animal model of inherited ALS.Proc Natl Acad Sci U S A,2008,105(40):15558-15563.