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doi: 10.1038/emboj.2013.53 80 MemczakSJensMElefsiniotiATortiFKruegerJRybakAet al

In the lysolecithin demyelination model, niacin treatment promotes phagocytosis of inhibitory myelin debris by microglia/macrophages, leading to increased numbers of oligodendrocyte progenitor cells in the lesion site and improved remyelination [8]

It is required for the biosynthesis of proteins, co-enzymes, prosthetic groups, vitamins, amino acids like Cys and Met, GSH, and secondary metabolites such as GSL and sulfoflavonoids