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J Neuroimmunol. 2018 Aug 15;321:61-65. doi: 10.1016/j.jneuroim.2018.05.016. Epub 2018 Jun 1.

Effects of vitamin D on axonal damage during de- and remyelination in the cuprizone model.

Author information

1
Norwegian Multiple Sclerosis Competence Centre, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Clinical Medicine, University of Bergen, Bergen, Norway. Electronic address: agnes.elisabeth.nystad@helse-bergen.no.
2
Norwegian Multiple Sclerosis Competence Centre, Department of Neurology, Haukeland University Hospital, Bergen, Norway; Department of Clinical Medicine, University of Bergen, Bergen, Norway. Electronic address: oivind.torkildsen@helse-bergen.no.
3
Norwegian Multiple Sclerosis Competence Centre, Department of Neurology, Haukeland University Hospital, Bergen, Norway. Electronic address: stig.wergeland@helse-bergen.no.

Abstract

Vitamin D deficiency is a risk factor for multiple sclerosis and associated with higher disease activity. The aim of this study was to investigate the effects of cholecalciferol and calcitriol on axonal damage during de- and remyelination in the cuprizone model. We found significantly less reduction of neurofilament immunopositive axons in the high vs. low cholecalciferol group, while high dose calcitriol, given during remyelination, did not influence axonal regeneration. Our results indicate that high dose vitamin D could protect against axonal loss in an experimental model for demyelination, if given before and during the demyelination.

KEYWORDS:

Axonal damage; Cuprizone; Demyelination; Multiple sclerosis; Remyelination; Vitamin D

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