缓慢扩大的病变与复发性多发性硬化症的疾病活动和灰质损失有关
Hiroaki Yokote1,2, Yusei Miyazaki3, Juichi Fujimori4
1Department of Neurology, Tokyo Metropolitan Komagome Hospital, Tokyo, Japan.
概括
在日本多发性硬化症 (MS) 患者中,缓慢扩张的病变 (SEL) 与疾病活动增加和大脑体积损失有关. SELs的数量可以作为MS进展的关键生物标志物.
科学领域:
- 神经学 神经学
- 放射学 放射学是一门学科.
- 神经免疫学 神经免疫学
背景情况:
- 缓慢扩张的病变 (SELs) 是多发性硬化症 (MS) 慢性活跃病变的新兴MRI标志物.
- SELs对大脑体积损失的影响及其在亚洲MS群体中的患病率尚不清楚.
- 这项研究侧重于日本MS患者,以澄清SELs的作用.
研究的目的:
- 在日本MS患者中调查SEL和没有疾病活动证据 (NEDA-3) 状态之间的关联.
- 在这个队列中确定SEL和大脑体积损失之间的关系.
- 探索SELs作为MS的潜在生物标志物.
主要方法:
- 在2年的时间内,对99名复发性多发性硬化症患者进行了回顾性评估.
- 使用纵向图像记录在串行大脑MRI上识别SEL.
- 使用逻辑回归和通用线性混合模型 (GLMMs) 的统计分析来评估SEL与疾病活动和大脑体积变化的关联.
主要成果:
- 在观察期间,35名患者 (35.4%) 发展出至少一个SEL.
- 多变量分析表明,≥2个SEL与获得NEDA-3地位的0.2倍风险有关.
- GLMMs显示SEL数量与皮质 (p=0.00169) 和皮下灰质 (p=0.00964) 的体积变化之间存在显著的负相关性.
结论:
- 在日本多发性硬化症患者中成功发现了SEL.
- SELs的数量与疾病活动相关,并有助于大脑体积损失.
- SEL显示出作为监测MS疾病活动的有价值生物标志物的潜力.
相关概念视频
01:19Multiple 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...
01:29Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
01:23Alzheimer 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...