The cuprizone model for demyelination

被引:254
作者
Torkildsen, O. [1 ,2 ]
Brunborg, L. A. [3 ]
Myhr, K. -M. [1 ,2 ]
Bo, L. [1 ,2 ]
机构
[1] Haukeland Hosp, Dept Neurol, Norwegian Multiple Sclerosis Competence Ctr, N-5021 Bergen, Norway
[2] Univ Bergen, Dept Clin Med, Neurol Sect, N-5020 Bergen, Norway
[3] Natl Inst Nutr & Seafood Res, Bergen, Norway
来源
ACTA NEUROLOGICA SCANDINAVICA | 2008年 / 117卷
关键词
cuprizone; demyelination; multiple sclerosis;
D O I
10.1111/j.1600-0404.2008.01036.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Background - Important advances in multiple sclerosis (MS) research have been made as a direct or indirect result of experiments in animal models for the disease, although MS is a disease only affecting humans. The cuprizone model is a model for toxic demyelination. In this model, young mice are fed with the copper chelator cuprizone, leading to oligodendrocyte death and a subsequent reversible demyelination. Spontaneous remyelination can be seen as early as 4 days after withdrawal of cuprizone. Materials and methods - This article reviews previous research on this model and discusses the potential of the model for future application in MS research. Discussion - The cuprizone model correlates with newer histopathological data in MS and is a valuable tool for studies on de- and remyelination. The use of the C57BL/6 strain offers the potential for future studies on transgene and knockout mice.
引用
收藏
页码:72 / 76
页数:5
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