漫画家关谷神奇总裁中西宏明PT -期刊文章盟盟——Hisatomo KOWA盟Hinako郎AU -中国人圆子盟Wataru SATAKE AU - Naonobu FUTAMURA AU - Itaru FUNAKAWA AU - Kenji JINNAI盟Motonori高桥AU -近藤武盟Yasuhiro上野盟Motoi神奈川AU - Kazuhiro小林盟Tatsushi户田拓夫TI -α-突触核蛋白寡聚物的广泛分布在多个系统萎缩的大脑被邻近结扎(p3.8 - 010) DP - 2019年4月09年TA -神经病学第六PG - p3.8 - 010 - 92 IP - 15补充4099 - //www.ez-admanager.com/content/92/15_supplement/p3.8 010. - 010.短4100 - //www.ez-admanager.com/content/92/15_supplement/p3.8 - -全所以Neurology2019 首页4月09年;92 AB -目的:揭示α-突触核蛋白(αS)低聚物的分布作为早期病理改变多系统萎缩(MSA)的大脑。背景:MSA神经病理学的标志是αS-positive胶质细胞质内含物(gci)。虽然严重的神经损失也观察到在MSA,神经细胞内含物(NIs)是罕见的gci相比,这样神经损失MSA的病理机制尚不清楚。gci和NIs晚期病理特征相对于αS寡聚物,不得代表MSA早期变化。披露的早期病理MSA,有必要检查αS聚合的早期,即。,αS寡聚物。设计/方法:我们采用了接近结扎试验(PLA)检查的分布αS寡聚物MSA患者脑组织中样本和其他疾病。这个研究包括5 MSA例(死亡年龄:73.8±8.3年,疾病持续时间:9.0±6.2年),5帕金森病(PD)的情况下(死亡年龄:76.4±6.3年,疾病持续时间:11.6±4.0年)疾病控制和5例(死亡年龄:63.6±9.6年,疾病持续时间:26.0±15.5年)。作为额外的控制,事后大脑样本4科目没有已知的神经系统疾病(死亡年龄:63.3±10.2年)。结果:MSA的大脑显示弥漫性分布和丰富的低聚物的积累αS大脑皮层的神经元和少突胶质细胞。在一些地区,寡聚αS信号强度与MSA的情况下高于与PD的情况下。 In contrast to previous studies, PLA revealed abundant αS oligomer accumulation in Purkinje cells in MSA brains, identifying oligomeric αS accumulation as a possible cause of Purkinje cell loss.Conclusions: The wide distribution of αS oligomers in MSA brain neurons has not been described previously and indicates a pathological mechanism of neuronal loss in MSA.Disclosure: Dr. Sekiya has nothing to disclose. Dr. Kowa has nothing to disclose. Dr. KOGA has nothing to disclose. Dr. TAKATA has nothing to disclose. Dr. Satake has nothing to disclose. Dr. Futamura has nothing to disclose. Dr. Funakawa has nothing to disclose. Dr. Jinnai has nothing to disclose. Dr. TAKAHASHI has nothing to disclose. Dr. KONDO has nothing to disclose. Dr. UENO has nothing to disclose. Dr. Kanagawa has nothing to disclose. Dr. Kobayashi has nothing to disclose. Dr. Toda has nothing to disclose.

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