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An animal model for late onset chronic demyelination disease caused by failed terminal differentiation of oligodendrocytes

机译：少突胶质细胞终末分化失败引起的迟发性慢性脱髓鞘疾病的动物模型

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Various animal models are available for studying human multiple sclerosis (MS). Most of them model the initial phase of MS, including the immune-triggered attack of the myelin membrane and/or oligodendrocytes and, occasionally, demonstrate the remission and relapsing phases. However, few mimic the late chronic demyelinating phase. Overexpression of the proteolipid protein gene (Plp) causes a unique demyelinating disorder in mice in which normal-appearing myelin forms early in life and chronic demyelination occurs later. We found that remyelination is severely affected in this late demyelinating phase, but is not caused by deprivation of oligodendrocyte progenitors expressing PDGF receptor alpha (PDGFR[alpha]) and Olig2, which are present at an even higher number in the demyelinated white matter of the mutants than in wild-type controls. Furthermore, mature oligodendrocytes containing PLP were observed, but failed to remyelinate. The ability of oligodendrocytes from older transgenic animals to produce a myelin membrane-like structure was not impaired when cultured in vitro, which indicates that the lack of remyelination is not simply caused by changes in the intrinsic properties of the oligodendrocytes.
机译：各种动物模型可用于研究人类多发性硬化症（MS）。他们中的大多数为MS的初始阶段建模，包括髓鞘膜和/或少突胶质细胞的免疫触发攻击，并偶尔显示缓解和复发阶段。但是，很少有人模仿晚期慢性脱髓鞘期。蛋白脂质蛋白基因（Plp）的过表达在小鼠中引起独特的脱髓鞘疾病，其中正常出现的髓磷脂在生命早期形成，而慢性脱髓鞘则在以后发生。我们发现，在该晚期脱髓鞘阶段，髓鞘再生受到严重影响，但不是由剥夺表达PDGF受体α（PDGFRα）和Olig2的少突胶质细胞祖细胞引起的，所述少突胶质祖细胞以更高的数量存在于脱髓鞘白质中。突变体比野生型对照。此外，观察到含有PLP的成熟少突胶质细胞，但未使髓鞘再生。当在体外培养时，来自较年长的转基因动物的少突胶质细胞产生髓磷脂膜样结构的能力并未受到损害，这表明缺乏再髓鞘化不是简单地由少突胶质细胞的内在特性引起的。

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