摘要
多发性硬化(MS)是未知病因的中枢神经系统(CNS)疾病。 MS变现为中枢神经系统炎症,脱髓鞘和轴突损伤的复杂病理生理学,使得它在实验系统的建模尤其困难。此外,MS不天然存在于其他物种这一证明已经进一步复杂了MS的临床前研究。这些年来,几个MS体内模型已经制定出来。实验性自身免疫性脑脊髓炎(EAE)代表了最广泛使用的MS实验模型,它依赖于自身免疫性范例来探索MS神经病理学。尽管已经了解EAE发生在神经炎症中的分子事件,不是所有的MS特点可以有效地在这个概念框架内塑造。因此,基于病毒感染或神经毒素管理的CNS脱髓鞘的可选模型已被表征。虽然不完美,但这些模型有很大的提高了我们免疫系统健康和疾病功能的知识。在另一边,他们与MS的固有的距离往往导致曲解和高估从这些实验系统中收集的数据。在这个综述里,每个模型将从其模仿MS的潜力和给患者带来最有希望治疗方法方面进行讨论。此外,我们将讨论的基因组技术如何帮助改进现有模型。
关键词: 多发性硬化症,脱髓鞘,实验性自身免疫性脑脊髓炎,自身免疫,cuprizone,卵磷脂,泰勒的小鼠脑脊髓炎病毒、鼠肝炎病毒。
Current Medicinal Chemistry
Title:Preclinical Models of Multiple Sclerosis: Advantages and Limitations Towards Better Therapies
Volume: 23 Issue: 14
Author(s): Alessandro Didonna
Affiliation:
关键词: 多发性硬化症,脱髓鞘,实验性自身免疫性脑脊髓炎,自身免疫,cuprizone,卵磷脂,泰勒的小鼠脑脊髓炎病毒、鼠肝炎病毒。
摘要: Multiple sclerosis (MS) is a disease of the central nervous system (CNS) with an unknown etiology. MS complex pathophysiology—characterized by CNS inflammation, demyelination and axonal injury—has made its modeling in experimental systems particularly problematic. Moreover, the evidence that MS does not naturally occur in other species has further complicated MS preclinical studies. Through the years, several MS in vivo models have been developed. Experimental autoimmune encephalomyelitis (EAE) represents the most widely used MS experimental model and relies upon the autoimmune paradigm to explore MS neuropathology. Although EAE has been instrumental in understanding the molecular events which take place upon neuroinflammation, not all MS hallmarks can be efficiently shaped within this conceptual frameshift. Thus, alternative models of CNS demyelination have been characterized, either based on viral infection or neurotoxin administration. However imperfect, these models have greatly improved our knowledge of the immune system's function in health and disease. On the other side, their intrinsic distance from MS has often led to misinterpreting and overestimating the data gleaned from these experimental systems. In this review, each model will be discussed in the light of its potentiality to mimic MS and translate the most promising therapies to patients. In addition, we will address how new genomic technologies can help improve the existing models.
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Cite this article as:
Alessandro Didonna , Preclinical Models of Multiple Sclerosis: Advantages and Limitations Towards Better Therapies, Current Medicinal Chemistry 2016; 23 (14) . https://dx.doi.org/10.2174/0929867323666160406121218
DOI https://dx.doi.org/10.2174/0929867323666160406121218 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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