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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Early axonal damage and progressive myelin pathology define the kinetics of CNS histopathology in a mouse model of multiple sclerosis
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Early axonal damage and progressive myelin pathology define the kinetics of CNS histopathology in a mouse model of multiple sclerosis

机译：早期轴突损伤和进行性髓鞘病理学定义了多发性硬化症小鼠模型中CNS组织病理学的动力学

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摘要

Studies of MS histopathology are largely dependent on suitable animal models. While light microscopic analysis gives an overview of tissue pathology, it falls short in evaluating detailed changes in nerve fiber morphology. The ultrastructural data presented here and obtained from studies of myelin oligodendrocyte glycoprotein (MOG):35-55-induced experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice delineate that axonal damage and myelin pathology follow different kinetics in the disease course. While myelin pathology accumulated with disease progression, axonal damage coincided with the initial clinical disease symptoms and remained stable over time. This pattern applied both to irreversible axolysis and early axonal pathology. Notably, these histopathological patterns were reflected by the normal-appearing white matter (NAWM), suggesting that the NAWM is also in an active neurodegenerative state. The data underline the need for neuroprotection in MS and suggest the MOG model as a highly valuable tool for the assessment of different therapeutic strategies.
机译：MS组织病理学的研究在很大程度上取决于合适的动物模型。尽管光学显微镜分析概述了组织病理学，但在评估神经纤维形态学的详细变化方面却不足。此处介绍的超微结构数据是从对C57BL / 6小鼠的髓鞘少突胶质细胞糖蛋白（MOG）：35-55诱导的实验性自身免疫性脑脊髓炎（EAE）的研究中获得的，表明轴突损伤和髓鞘病理在疾病过程中遵循不同的动力学。虽然髓磷脂病理随着疾病的进展而累积，但轴突损伤与最初的临床疾病症状相吻合，并且随着时间的推移保持稳定。这种模式既适用于不可逆的溶栓作用，也适用于早期的轴突病理学。值得注意的是，这些组织病理学模式由正常出现的白质（NAWM）反映出来，表明NAWM也处于活跃的神经退行性状态。数据强调了MS中神经保护的必要性，并建议MOG模型作为评估不同治疗策略的极有价值的工具。

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