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[轴突退变在多发性硬化发病机制中的作用]

[Axonal degeneration in the pathogenesis of multiple sclerosis].

作者信息

Mirowska Dagmara, Członkowska Anna

机构信息

II Kliniki Neurologii Instytutu Psychiatrii i Neurologii w Warszawie.

出版信息

Neurol Neurochir Pol. 2002 Jul-Aug;36(4):777-89.

Abstract

Axonal degeneration plays an important role in the cumulation of disability in patients with multiple sclerosis (MS). Pathological studies have demonstrated axonal damage, particularly in area of acute inflammation and demyelination, and in chronic lesions. The mechanism of axonal loss is uncertain, but may involve axonal degeneration which is secondary to demyelination. Mediators of inflammation, including cytokines and proteolytic enzymes may be responsible for axonal damage, as may be nitric oxide. Moreover, axonal destruction might be due to immune cells attack directed to axonal components. The method to evaluate the intensity of cerebral and spinal cord atrophy, both reflecting axonal damage, is still searched. It is thought that therapy affecting the axonal destruction would possibly reduce progression of disability in MS patients.

摘要

轴突变性在多发性硬化症(MS)患者的残疾累积中起重要作用。病理研究已证实存在轴突损伤,尤其是在急性炎症和脱髓鞘区域以及慢性病变中。轴突丧失的机制尚不确定,但可能涉及继发于脱髓鞘的轴突变性。包括细胞因子和蛋白水解酶在内的炎症介质可能是轴突损伤的原因,一氧化氮也可能如此。此外,轴突破坏可能是由于针对轴突成分的免疫细胞攻击。目前仍在寻找评估脑和脊髓萎缩程度的方法,脑和脊髓萎缩均反映轴突损伤。人们认为,影响轴突破坏的治疗可能会减少MS患者残疾的进展。

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