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Christian Cordano¹, Sebastian Werneburg², Ahmed Abdelhak³

¹UCSF Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, San Francisco, CA, USA; Department of Neurology, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy; IRCCS Ospedale Policlinico San Martino, Genoa, Italy.

Cell reports. Medicine

|April 4, 2024

概括

突触损伤,通过内部状层 (IPL) 的稀薄来检测,在多发性硬化症 (MS) 中的残疾进展之前. 这一发现为跟踪多发性硬化患者的疾病进展和功能衰退提供了潜在的生物标志物.

科学领域:

神经科学是一个神经科学.
眼科医生眼科眼科
免疫学免疫学免疫学

背景情况:

神经退行导致多发性硬化症 (MS) 的永久性残疾.
目前用于MS进展的生物标志物不足.
突触损伤越来越被认为是神经退行性疾病的早期事件.

研究的目的:

研究突触损伤作为多发性硬化症 (MS) 进展的早期生物标志物.
为了确定内状层 (IPL) 稀薄是否预测MS的功能衰退.
探索MS中脱髓化,质激活,突触损失和神经轴损伤之间的关系.

主要方法:

利用慢性多发性硬化症的动物模型研究突触损伤.
分析了12年来800多名多发性硬化患者的视网膜成像数据 (IPL厚度).
进行了血液蛋白质组范围的分析,以将分子标记与疾病病理学相关联.

主要成果:

在多发性硬化动物模型中,通过IPL稀释证明的突触损伤,在神经元损失和症状发作之前.
发现IPL缩直接先于人类MS参与者的临床进展.
血液蛋白质组分析显示了脱髓化,质激活和突触损失之间的相关性,独立于神经轴损伤.

结论:

内状层 (IPL) 的稀薄是多发性硬化症 (MS) 进展的潜在早期生物标志物.
突触损失是MS功能衰退的关键驱动因素,可以非侵入性监测.
监测突触损伤提供了一个生物学相关的方法来理解和预测多发性硬化症的进展.

关键词:

欧洲电子商务管理局 (EEAE)血液中的生物标志物脱化是脱化的一种.实验性的自身免疫性脑膜炎.光学连贯性断层扫描技术视网膜视网膜视网膜是一个血清蛋白质组的血清蛋白质组是发生突触损伤的突触损伤.

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