Axonal and neuronal degeneration in multiple sclerosis: mechanisms and functional consequences
Axonal and neuronal degeneration in multiple sclerosis: mechanisms and functional consequences
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DOI：
10.1097/00019052-200106000-00003
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发表时间：
2001-06-01
影响因子：
4.8
通讯作者：
Trapp, BD
中科院分区：
文献类型：
--
作者：
Bjartmar, C;Trapp, BD
对多发性硬化症中轴突损伤的重新关注已显著地将该疾病的研究重点转向神经变性。在过去的一年中，磁共振和形态学研究继续证实并扩展了轴突横断始于疾病发病的概念，并且累积的轴突损失为大多数长期MS患者经历的进行性残疾提供了病理基础。尽管炎症和慢性脱髓鞘可能是轴突横断的原因，但对所涉及的分子机制知之甚少。MS也可以被认为是一种炎症性神经退行性疾病，这一观点对治疗方法、患者监测和未来的治疗策略具有重要的临床意义。中国医学杂志，2004,14 (3):391 - 391 (C)。
Renewed interest in axonal injury in multiple sclerosis has significantly shifted the focus of research into this disease toward neurodegeneration. During the past year magnetic resonance and morphologic studies have continued to confirm and extend the concept that axonal transection begins at disease onset, and that cumulative axonal loss provides the pathologic substrate for the progressive disability that most long-term MS patients experience, Although inflammation and chronic demyelination are probable causes of axonal transection, little is known about the molecular mechanisms that are involved, The view that MS can also be considered an inflammatory neurodegenerative disease has important clinical implications for therapeutic approaches, monitoring of patients, and future treatment strategies. Curr Opin Neurol 14:271-278 (C) 2001 Lippincott Williams & Wilkins.