From http://www.benthamscience.com/open/todd ... ODDISJ.pdf
Niacin plays an important role in myelination associated with the synthesis of cerebrosides which contain high levels of long chain fatty acid [77, 78]. Niacin activates the G-protein coupled receptor GPR109a to produce the IDO- inducing tolerogenic prostaglandins PGE (2) and PGD (2). PGD (2) is converted to the anti-inflammatory prostaglandin. These prostaglandins exert potent anti-inflammatory activities . Niaspan treatment experimental autoimmune encephalomyelitis (EAE) mice significantly reduce inflammatory infiltrates and demyelination areas, and stimulate oligodendrogenesis and axonal regeneration . Neurological functional recovery was significantly increased when treatment of EAE mice with niaspan starting on the immunization or clinical onset day . In addition, nicotinamide, an NAD biosynthesis precursor, profoundly prevents the degeneration of demyelinated axons and improves the behavioral deficits in EAE models . Nicotinamide profoundly ameliorates and prevents autoimmune-mediated demyelination in EAE via maintaining levels of NAD, without activating PPAR nor any G-protein-coupled receptor . Therefore, niacin and nicotinamide may be a target for MS treatment.