Molecular mechanisms of neuronal apoptosis in chronic inflammatory CNS diseases

R. Diem, Muriel B. Sättler, K. Maier, M. Bähr
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引用次数: 3

Abstract

In the adult CNS, apoptosis of neuronal populations contributes to manifestation of clinical symptoms during several neurodegenerative disorders. In multiple sclerosis (MS), an inflammatory demyelinating CNS disease, neurodegeneration has long been thought to occur secondary and late during clinical course. However, in the last years, post-mortem studies of human brain tissue as well as data from animal models have shown that apoptosis of neurons reaches a significant extent already in the early stages of the disease. As neurodegeneration in MS correlates with permanent neurological deficits in patients, understanding the mechanisms would be an important pre-condition for designing appropriate neuroprotective therapies. This review article gives an overview about current data concerning features and molecular mechanisms of neuronal apoptosis in chronic inflammatory autoimmune CNS diseases. Furthermore, possible implications for the development of neuroprotective therapies are discussed.
慢性炎症性中枢神经系统疾病中神经元凋亡的分子机制
在成人中枢神经系统中,一些神经退行性疾病的临床症状与神经元群的凋亡有关。多发性硬化症(MS)是一种炎症性脱髓鞘性中枢神经系统疾病,长期以来,人们一直认为神经退行性变发生在临床过程的继发性和晚期。然而,在过去的几年里,对人类脑组织的死后研究以及动物模型的数据表明,在疾病的早期阶段,神经元的凋亡已经达到了很大程度。由于多发性硬化症的神经变性与患者的永久性神经功能缺损相关,了解其机制将是设计适当的神经保护疗法的重要先决条件。本文综述了慢性炎症性自身免疫性中枢神经系统疾病中神经元凋亡的特征和分子机制。此外,对神经保护疗法的发展可能产生的影响进行了讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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