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

08:00 EDT 15th August 2018 | BioPortfolio

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

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.

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Journal Details

This article was published in the following journal.

Name: Journal of neuroimmunology
ISSN: 1872-8421
Pages: 61-65

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Copper chelator that inhibits monoamine oxidase and causes liver and brain damage.

A lipid cofactor that is required for normal blood clotting. Several forms of vitamin K have been identified: VITAMIN K 1 (phytomenadione) derived from plants, VITAMIN K 2 (menaquinone) from bacteria, and synthetic naphthoquinone provitamins, VITAMIN K 3 (menadione). Vitamin K 3 provitamins, after being alkylated in vivo, exhibit the antifibrinolytic activity of vitamin K. Green leafy vegetables, liver, cheese, butter, and egg yolk are good sources of vitamin K.

Statistical formulations or analyses which, when applied to data and found to fit the data, are then used to verify the assumptions and parameters used in the analysis. Examples of statistical models are the linear model, binomial model, polynomial model, two-parameter model, etc.

A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)

OXIDOREDUCTASES which mediate vitamin K metabolism by converting inactive vitamin K 2,3-epoxide to active vitamin K.

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