The findings reveal that taurine could be could be added to an MS therapy regimen to boost mature oligodendrocyte production, and in turn, remyelination.
Luke Lairson, PhD, assistant professor of chemistry at The Scripps Research Institute
Luke Lairson, PhD
The current scope of remyelination-promoting therapies for patients with multiple sclerosis (MS) may have gotten a boost from a newly discovered process out of The Scripps Research Institute (TSRI).1
The research suggests that taurine could be added to an MS therapy regimen in order to boost mature oligodendrocyte production, and therefore remyelination. In doing so, the hope is it would ultimately reduce relapses for patients with MS.
A group of scientists out of the institute, including Luke Lairson, PhD, assistant professor of chemistry at TSRI, and Gary Siuzdak, PhD, senior director of TSRI’s Scripps Center for Metabolomics and a professor of chemistry, and molecular and computational biology, has uncovered that metabolite taurine, in combination with benztropine and miconazole, can greatly enrich the conversion of oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes. Once matured, these cells produce myelin, which helps in repairing damages nerves in those with MS.
Lairson told NeurologyLive’s sister publication, MD Magazine, that taurine was identified as a result of a process that gauged levels of polar and non-polar metabolites present in OPCs versus mature oligodendrocytes. Taurine will not improve remyelination on its own, but it appears to act as a booster for therapies that induce the process.
“Identified metabolites that were present at different amounts were then screened, alone and in combination, to determine the ability of endogenous metabolites to impact the process of oligodendrocyte differentiation and/or maturation,” Lairson said.
During that screening, it was apparent that taurine levels were higher during the oligodendrocyte differentiation and maturation, which impelled the investigators to look into it. “Levels of taurine, an aminosulfonic acid possessing pleiotropic biological activities and broad tissue distribution properties, were found to be significantly elevated (∼20-fold),” they wrote.
“Taurine was the primary target metabolite since the change during differentiation was so significant and since creatine—another significantly altered metabolite—was already in our standard medium,” Siuzdak said. Although, he noted that it’s possible there are other metabolites that could provide more benefit.
The team suggested that taurine’s benefit it derived from its ability to directly increase the availability of serine pools—the foundation for the “synthesis of the glycosphingolipid components of myelin that define the functional oligodendrocyte cells state,” they wrote.
The real impact, though, is that taurine is not only readily available on the market and affordable—a bottle of 1 g goes for around $10, Siuzdak said—but is naturally produced in the body. It is orally available and actively transported into the central nervous system, Lairson said. It is present in products and supplements, such as energy drinks, and is found in most diets.
“It is generally regarded as safe and could be readily supplemented to the diet of patients if deemed safe and effective in relevant animal efficacy and toxicity models,” Lairson said.
The team noted that taurine “is found in the brain at millimolar concentrations and it is a very well-tolerated agent that is actively transported across the blood-brain barrier.” As such, they admitted their belief that supplementation, in combination with the existing standard of care drugs, with taurine could be a feasible strategy of remyelination improvement through the enhancement of glycosphingolipid biosynthesis in oligodendrocytes. And, though taurine already has a good track record of safety, the next step is to use rodent models to confirm the study’s findings—work Lairson said is underway.
The new study is part of ongoing research into MS by TSRI. Institute researchers, including Lairson, first showed the benztropine can help OPCs mature into oligodendrocytes. Benztropine was previously approved as a Parkinson’s disease drug.
1. Beyer BA, Fang M, Sadrian B, et. al.
discovery of a metabolite that enhances oligodendrocyte maturation. Nat Chem Biol. 2018;14(1):22-28.