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Working with an animal model of MS as well as human post-mortem brains, the researchers found that fingolimod suppresses neuroinflammation by functionally and physically regulating B 12 communication pathways, specifically elevating a B 12 receptor called CD320 needed to take up and use needed B 12 when it is bound to TCN2, which distributes B 12 throughout the body, including the CNS

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