[多发性硬化治疗中的神经保护作用]

[Neuroprotection in the treatment of multiple sclerosis].

作者信息

Zipp F, Gold R

机构信息

Klinik und Poliklinik für Neurologie, Universitätsmedizin Mainz, Johannes-Gutenberg-Universität, Langenbeckstr. 1, 55131 Mainz, Deutschland.

出版信息

Nervenarzt. 2011 Aug;82(8):973-7. doi: 10.1007/s00115-011-3262-2.

Abstract

Atrophy, the wasting or shrinkage of tissue, of the nervous system is the main feature of neurodegeneration, i.e. the umbrella term for the progressive loss of structure or function of neurons. Loss of neurons due to cell death and axonal degeneration characterize neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease or amyotrophic lateral sclerosis. In these illnesses, it still has to be elucidated to which extent inflammation is part of the pathology. Conversely, in chronic inflammation of the central nervous system (CNS), atrophy has previously also been described and neurodegeneration is discussed as a pathologic feature. The most frequent chronic inflammatory disease of the CNS is multiple sclerosis (MS), which leads to devastating relapsing-remitting symptoms and disability during the relapses, increasingly during the course of disease in patients. Meanwhile it became clear that axons already reveal pathology early in the disease and neurons are affected in the cortex and the spinal cord, albeit to a different extent. The broadening of understanding neurodegenerative aspects of MS pathology demands and creates new therapeutic strategies. Current medication used in MS treatment as well as medications about to be approved are primarily anti-inflammatory therapies. By modulating the immune system and thereby blocking key steps of the pathology, the immunomodulation therapies in MS have a slight impact on disability progression. There is, however, clinical and experimental data concerning the potential neuroprotective properties of novel therapies. Combining anti-inflammatory and direct neuroprotective or even neuroregenerative therapy strategies would be a step forward in the treatment of multiple sclerosis.

摘要

萎缩,即组织的消瘦或萎缩,是神经系统神经退行性变的主要特征,神经退行性变是神经元结构或功能进行性丧失的统称。因细胞死亡和轴突退变导致的神经元丧失是阿尔茨海默病、帕金森病或肌萎缩侧索硬化等神经退行性疾病的特征。在这些疾病中,炎症在多大程度上是病理学的一部分仍有待阐明。相反,在中枢神经系统(CNS)的慢性炎症中,先前也已描述过萎缩,并且神经退行性变被作为一种病理特征进行讨论。中枢神经系统最常见的慢性炎症性疾病是多发性硬化症(MS),它会导致严重的复发 - 缓解症状,并且在复发期间,尤其是在疾病过程中,患者的残疾情况会日益加重。与此同时,已经明确轴突在疾病早期就已出现病理变化,并且神经元在皮质和脊髓中受到影响,尽管程度不同。对多发性硬化症病理神经退行性方面认识的拓宽需要并催生了新的治疗策略。目前用于治疗多发性硬化症的药物以及即将获批的药物主要是抗炎疗法。通过调节免疫系统从而阻断病理过程的关键步骤,多发性硬化症的免疫调节疗法对残疾进展有轻微影响。然而,有关于新疗法潜在神经保护特性的临床和实验数据。将抗炎与直接的神经保护甚至神经再生治疗策略相结合将是多发性硬化症治疗向前迈出的一步。

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