Fingolimod does not enhance cerebellar remyelination in the cuprizone model

被引:26
作者
Alme, Maria Nordheim [1 ]
Nystad, Agnes E. [2 ,3 ]
Bo, Lars [1 ,2 ,3 ]
Myhr, Kjell-Morten [1 ,2 ,3 ]
Vedeler, Christian A. [1 ,3 ,4 ]
Wergeland, Stig [2 ,3 ]
Torkildsen, Oivind [1 ,2 ,3 ]
机构
[1] Univ Bergen, Dept Clin Med, N-5020 Bergen, Norway
[2] Haukeland Hosp, Dept Neurol, Norwegian Multiple Sclerosis Competence Ctr, N-5021 Bergen, Norway
[3] Univ Bergen, Dept Clin Med, Kristian Gerhard Jebsen MS Res Ctr, N-5020 Bergen, Norway
[4] Haukeland Hosp, Dept Neurol, N-5021 Bergen, Norway
关键词
FTY720; Fingolimod; Cuprizone; Cerebellum; Demyelination; Remyelination; MULTIPLE-SCLEROSIS; CORTICAL DEMYELINATION; FTY720; RECEPTOR; PEDUNCLE; SURVIVAL; MATTER; WHITE; GREY;
D O I
10.1016/j.jneuroim.2015.06.006
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Fingolimod (FTY720) is approved for treatment of relapsing-remitting multiple sclerosis. In vitro studies have found that fingolimod stimulates remyelination in cerebellar slices, but in vivo animal studies have not detected any positive effect on cerebral remyelination. The discrepant findings could be a result of different mechanisms underlying cerebral and cerebellar remyelination. The cuprizone model for de- and remyelination was used to evaluate whether fingolimod had an impact on cerebellar remyelination in vivo. We found that fingolimod did not have any effect on cerebellar remyelination, number of mature oligodendrocytes, microglia or astrocytes when fed after cuprizone exposure. (C) 2015 The Authors. Published by Elsevier B.V.
引用
收藏
页码:180 / 186
页数:7
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