异常补充激活与多发性硬化症中结构性脑损伤有关
Johanna Oechtering1,2, Sabine Anna Schaedelin2,3, Kerstin Stein4
1Department of Neurology, University Hospital and University of Basel.
Neurology(R) neuroimmunology & neuroinflammation
|January 3, 2025
概括
脑脊液中补充剂的激活与多发性硬化症 (MS) 的进展和大脑损伤有关. 针对补充系统可能有助于减少MS相关的残疾.
科学领域:
- 神经免疫学 神经免疫学
- 补充系统生物学 补充系统生物学
- 神经学 神经学
背景情况:
- 脑脊液 (CSF) 中补充蛋白水平升高与多发性硬化症 (MS) 严重程度相关.
- 了解补充激活和多发性硬化病活动之间的关系对于治疗开发至关重要.
研究的目的:
- 调查CSF中的补充激活配置文件是否与MS疾病活动和进展的定量MRI指标和液体生物标志物相关.
- 确定特定补充成分与神经退行症和MS炎症标志物之间的关联.
主要方法:
- 在112名临床隔离综合征患者和127名多发性硬化症患者的CSF中量化了12种补充成分和激活产品.
- 评估了纵向MRI和量化液体生物标志物,包括神经丝光链,GFAP,CXCL-13,CXCL-9和IL-12b.
- 利用多变量模型分析补充参数和MRI/生物标志物结果之间的关联.
主要成果:
- 补充成分C4a,Ba和C3a与加速的大脑缩和T2加权损伤体积增加密切相关.
- C3a和Ba与更高的对比增强病变 (CEL) 几率和偏磁边缘病变 (PRL) 的发病率增加相关.
- C1q,C3a和C4a与质纤维酸蛋白 (GFAP) 水平升高有关,这表明神经炎症.
结论:
- 内补体激活与MRI指标和MS疾病活动和进展的生物标志物一致相关.
- 异常补充激活与MS中的结构性脑损伤有显著的相关性.
- 针对补充系统提出了一个潜在的治疗策略,以减轻MS中残疾积累.
相关概念视频
Complement System
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...
Multiple Sclerosis l: Introduction
Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...


