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Fingolimod does not enhance cerebellar remyelination in the cuprizone model.

Journal of neuroimmunology (2015-07-23)
Maria Nordheim Alme, Agnes E Nystad, Lars Bø, Kjell-Morten Myhr, Christian A Vedeler, Stig Wergeland, Øivind Torkildsen
ZUSAMMENFASSUNG

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.

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Sigma-Aldrich
Monoklonaler Anti-GFAP-Antikörper (Glial Fibrillary Acidic Protein, Saures Gliafaserprotein) in Maus hergestellte Antikörper, clone G-A-5, ascites fluid
Sigma-Aldrich
Anti-Neurofilament 70-kDa-Antikörper, Klon DA2, culture supernatant, clone DA2, Chemicon®
Sigma-Aldrich
Anti-Neuriten-Auswuchs-Inhibitor A-Antikörper, Chemicon®, from rabbit