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dc.contributor.authorAlme, Maria Nordheimen_US
dc.contributor.authorNystad, Agnes Elisabethen_US
dc.contributor.authorBø, Larsen_US
dc.contributor.authorMyhr, Kjell-Mortenen_US
dc.contributor.authorVedeler, Christian A.en_US
dc.contributor.authorWergeland, Stigen_US
dc.contributor.authorTorkildsen, Øivinden_US
dc.date.accessioned2016-01-11T10:20:20Z
dc.date.available2016-01-11T10:20:20Z
dc.date.issued2015-08
dc.PublishedJournal of Neuroimmunology 2015, 285:180-186eng
dc.identifier.issn0165-5728
dc.identifier.urihttps://hdl.handle.net/1956/10915
dc.description.abstractFingolimod (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.en_US
dc.language.isoengeng
dc.publisherElseviereng
dc.rightsAttribution CC BY-NC-NDeng
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/eng
dc.subjectFTY720eng
dc.subjectFingolimodeng
dc.subjectCuprizoneeng
dc.subjectCerebellumeng
dc.subjectDemyelinationeng
dc.subjectRemyelinationeng
dc.titleFingolimod does not enhance cerebellar remyelination in the cuprizone modelen_US
dc.typeJournal article
dc.date.updated2015-12-22T10:39:12Z
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2015 The Authors
dc.identifier.doihttps://doi.org/10.1016/j.jneuroim.2015.06.006
dc.identifier.cristin1291743


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