POTENTIAL ROLE OF BUPRENORPHINE IN MULTIPLE SCLEROSIS REMYELINATIONTHERAPY

SANCHEZ ES; BIGBEE J; ROBINSON S; SATO-BIGBEE C; ALVAREZ SE

Congreso; 48th Annual Meeting Argentine Society for Biochemistry and Molecular Biology; 2012

Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the Central Nervous System (CNS). Remyelination is performed by oligodendrocyte progenitors to prevent axonal loss. In MS, the insufficiency of remyelination leads to the irreversible degeneration of axons which correlates with clinical decline. Therefore, the development of a regenerative strategy to promote remyelination is crucial in MS management. Though the immunological effects of FTY720 (fingolimod), the first oral therapy approved for the treatment of MS, are well established, there is controversy about its contribution on myelin repair. In that regard, while FTY720 inhibits the infiltration of lymphocytes and prevents MS progression, our previous results established that also arrests the differentiation of oligodendrocytes, inhibiting the potential remyelination. On the other hand, we have also revealed that opioid signaling regulates myelination. Here, we show that buprenorphine, an opioid analogue used for pain and addiction treatment, increases the expression of myelin basic proteins, accelerates oligodendrocyte development and induces oligodendrocyte differentiation . These evidences suggest that buprenorphine could be considered as a complementary therapy of FTY720 to promote remyelination and to prevent neuronal irreversible damage in patients suffering fromMS