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Augmenting brain B 12 with fingolimod or potentially related molecules could enhance both current and future MS therapies. In their paper, the team at Sanford Burnham Prebys, with collaborators at University of Southern California, Juntendo University in Japan, Tokyo University of Pharmacy and Life Sciences and State University of New York, focused on the molecular functioning of FTY720 or fingolimod (Gilenya), a sphingosine 1-phosphate (S1P) receptor modulator that suppresses distribution of T and B immune cells errantly attacking the brains of MS patients

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The key pathway for the development of these neurological symptoms is odd chain fatty acid breakdown