Passa al contenuto
Merck

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
ABSTRACT

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.

MATERIALI
N° Catalogo
Marchio
Descrizione del prodotto

Sigma-Aldrich
Monoclonale Anti-proteina acida gliale fibrillare (GFAP), clone G-A-5, ascites fluid
Sigma-Aldrich
Anticorpo anti-neurofilamento di 70 kDa, clone DA2, culture supernatant, clone DA2, Chemicon®
Sigma-Aldrich
Anti-Neurite Outgrowth Inhibitor A Antibody, Chemicon®, from rabbit