TY -的T1 - MS患者CSF引起线粒体功能障碍在神经学无髓鞘的神经文化(P05.179) JF -乔-神经病学SP - P05.179 LP - P05.179六世- 80 - 7补充AU - Ilana Katz沙非盟-奥斯卡Vi首页daurre AU -杰弗瑞海恩斯盟Kadidia Adula AU -科里麦格劳盟安吉拉Vidal-Jordana盟-卡洛斯Pardo-Villamizar AU -彼得·卡拉布雷西AU -弗雷德·卢布林盟亚伦米勒AU -梅里纳Varghese盟朱利奥Pasinetti盟Patrizia Casaccia Y1 - 2013/02/12 UR - //www.ez-admanager.com/content/80/7_Supplement/P05.179.abstract N2 -目的:确定MS患者的CSF对神经元线粒体功能的影响。背景:轴突和神经元损伤永久性残疾的MS患者至关重要。氧化应激中起着重要作用在轴突和神经元损伤线粒体功能受损和后续能源失败。研究在人类样本表明,MS患者的CSF可能调节线粒体功能,因此导致疾病进展的。设计/方法:我们比较脑脊液从19 MS患者和9控制调节线粒体功能的能力的主要文化无髓鞘的大鼠海马神经元有或没有慢性暴露于亚阈值水平的氧化应激。生物能量学参数评估使用海马XF24细胞外流量分析仪(海马生物科学);线粒体活性研究是由体内染色与水户跟踪(表达载体)。结果:培养健康的神经元与MS患者CSF诱导改变精力充沛的概要文件的耗氧率(OCR)和细胞外酸化率(ECAR),但保留细胞应对压力的能力。脑脊液从MS患者线粒体活性的降低和诱导氧化应激,提高硝基酪氨酸所示的水平。在chronically-stressed神经元文化中,MS患者CSF诱导减少30±10% OCR的细胞应对压力的能力。结论:这项研究表明,MS患者的CSF增加健康的神经元响应的能量需求增强线粒体功能。 The same CSF on chronically stressed neurons, however, induces severe impairment; these cells are unable to supply and match the increased energetic demand. These experiments support the concept of increased energetic demand in the MS brain. Future directions include large-scale proteomic study of CSF samples to identify candidate targets for neuroprotection, biomarkers for diagnosis/prognosis, and further exploration of correlations to clinical disease.Supported by: Grant from the National Multiple Sclerosis Society (RG-4134-A9). Dr. Katz Sand's fellowship is supported by a Sylvia Lawry Grant from the National Multiple Sclerosis Society. Dr. Haines is supported by a fellowship from the Multiple Sclerosis Society of Canada and the Fonds de la Recherche en Sante du Quebec.Disclosure: Dr. Katz has nothing to disclose. Dr. Vidaurre has nothing to disclose. Dr. Haines has nothing to disclose. Dr. Adula has nothing to disclose. Dr. McGraw has received personal compensation for activities with Biogen Idec. Dr. Vidal-Jordana has nothing to disclose. Dr. Pardo-Villamizar has nothing to disclose. Dr. Calabresi has received personal compensation for activities with Biogen Idec, Teva Neuroscience, Genzyme Corporation, Vaccinex, Vertex, and Novartis. Dr. Calabresi has received research support from the National Institutes of Health, the National Multiple Sclerosis Society, Nancy Davis Foundation, Biogen Idec, Vertex, Genentech, Inc., Abbott, and Bayer. Dr. Lublin has received personal compensation for consulting from Bayer HealthCare Pharmaceuticals, Biogen Idec, EMD Serono Inc., Novartis, Pfizer, Teva Neuroscience, Genmab, Medicinova, Actelion, Sanofi-Aventis, Acorda, Questcor, Roche, Celgene, Abbott, Johnson & Johnson, Revalesio, Coronado Bioscience, and GenFL. Dr. Lublin has received compensation from Elsevier for serving as Co-Chief Editor of Multiple Sclerosis and Related Diseases. Dr. Miller has received personal compensation for activities with Acorda Therapeutics, Biogen Idec, GlaxoSmithKline, Merck Serono, Novartis, Nuron Biotech, ONO, Genzyme/Sanofi, Questcor, Teva Neuroscience, and Accordant Health Services. Dr. Miller has received personal compensation for activities in an editorial capacity for Continuum and Continuum Audio. Dr. MIller has received research support from Acorda, Biogen Idec, Genentech, Genzyme/sanofi-aventis, Novartis, and Roche. Dr. Varghese has nothing to disclose. Dr. Pasinetti has nothing to disclose. Dr. Casaccia has nothing to disclose.Wednesday, March 20 2013, 2:00 pm-7:00 pm ER -