Inflammatory demyelination is not central to the pathogenesis of multiple sclerosis
Inflammatory demyelination is not central to the pathogenesis of multiple sclerosis
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DOI：
10.1007/s00415-005-5003-6
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发表时间：
2005-11-01
影响因子：
6
通讯作者：
Brück, W
中科院分区：
文献类型：
--
作者：
Brück, W
多发性硬化症是一种中枢神经系统疾病，它会破坏髓磷脂、少突胶质细胞、神经元和轴突。历史上认为是由自身免疫过程引起的，主要影响白质中的髓鞘和少突胶质细胞，最近的数据提供证据表明，一个全身性、弥漫性神经退行性过程在ms的发病机制中起重要作用。在活动性脱髓鞘病变中存在高密度的轴突横断，但在非活动性斑块中也存在持续的低水平轴突损伤，以及整个神经系统的弥漫性轴突和神经元损失。最初的轴索损伤似乎与炎症密切相关，但并不局限于病变本身。损伤可通过顺行、逆行或跨突触变性在整个神经系统中传播。灰质和白质的累积性组织损失，特别是轴突的累积性组织损失是重要的，并且可能是不可逆神经功能障碍积累和转化为进行性疾病过程的主要决定因素。
Multiple sclerosis is a disease of the central nervous system that destroys myelin, oligodendrocytes, neurons and axons. Historically considered to be caused by an autoimmune process mainly affecting myelin and oligodendrocytes in the white matter, recent data provide evidence that a generalized, diffuse neurodegenerative process plays an important role in the pathogenesis of MS. There is a high density of axonal transections in active demyelinating lesions, but also persistent low-level axonal damage in inactive plaques and diffuse axonal and neuronal loss throughout the nervous system. Initial axonal injury appears to be closely related to inflammation, but is not restricted to the lesions themselves. Damage may be propagated throughout the nervous system by anterograde Wallerian, retrograde or transynaptic degeneration. Cumulative tissue loss in the grey and white matter, especially of axons, is important and probably the principal determinant of accumulation of irreversible neurological disability and of conversion to a progressive disease course.