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多发性硬化症中的炎症与变性

Inflammation and degeneration in multiple sclerosis.

作者信息

Brück W, Stadelmann C

机构信息

Department of Neuropathology, Georg-August-Universität Göttingen, Robert-Koch-Strasse 40, D-37075, Göttingen, Germany.

出版信息

Neurol Sci. 2003 Dec;24 Suppl 5:S265-7. doi: 10.1007/s10072-003-0170-7.

Abstract

Multiple (MS) sclerosis is a chronic inflammatory demyelinating disease of the central nervous system with the pathological hallmarks of inflammation, demyelination, axon loss and gliosis. In the initial relapsing-remitting phase of the disease, the inflammatory-demyelinating component seems to predominate, whereas the progressive disease appears to be characterized by a neurodegenerative component leading to extensive neuroaxonal damage in the MS brain. Axon loss most likely determines the persistent neurological deficit in progressive MS. Recent studies pointed out that axon damage occurs early in the disease and during lesion development. Two different phases of axon degeneration were characterized, the first occurring during active myelin breakdown and the second in chronic demyelinated plaques in which the naked axon seems more susceptible to further damage. The exact mechanisms and effector molecules of axonal degeneration, however, are not yet defined, and an axon-protective therapy has not yet been established.

摘要

多发性硬化症是一种中枢神经系统的慢性炎症性脱髓鞘疾病,具有炎症、脱髓鞘、轴突丧失和胶质增生等病理特征。在疾病的初始复发缓解期,炎症脱髓鞘成分似乎占主导,而进展性疾病似乎以神经退行性成分为特征,导致多发性硬化症患者大脑中广泛的神经轴突损伤。轴突丧失很可能决定了进展性多发性硬化症中持续的神经功能缺损。最近的研究指出,轴突损伤在疾病早期和病变发展过程中就会发生。轴突变性可分为两个不同阶段,第一个阶段发生在活跃的髓鞘破坏期间,第二个阶段发生在慢性脱髓鞘斑块中,其中裸露的轴突似乎更容易受到进一步损伤。然而,轴突变性的确切机制和效应分子尚未明确,且尚未建立轴突保护疗法。

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