An already approved medication used for bladder problems might help to treat multiple sclerosis, according to researchers at the State University of New York at Buffalo.
Lead author Fraser J. Sim, PhD, Assistant Professor in the Department of Pharmacology and Toxicology in the University at Buffalo School of Medicine and Biomedical Sciences stated “We have identified a new drug target that promotes stem cell therapy for myelin-based disease, such as MS.”
The medication is called solifenacin, which has already been approved by the federal drug administration (FDA) to treat overactive bladder. The drug targets a receptor for the neurotransmitter acetylcholine, known as the muscarinic receptor. It could also act on cells that remyelinate the nerves of the body. Myelin is the fatty substance that wraps around neurons and is damaged in multiple sclerosis due to an autoimmune attack. Oligodendocytes are specialized cells that produce the myelin.
“Our hypothesis is that in MS, the oligodendrocyte progenitor cells seem to get stuck,” Sim noted. “When these cells don’t mature properly, they don’t differentiate into myelinating oligodendrocytes.”
In the study, Sim and his coworkers studied the molecular pathways that control how oligodendrocyte cells formed. Then they tried to identify drugs that could change how much myelin the oligodendrocytes produce.
They noted that when drugs that bound to the muscarinic type 3 receptor on human oligodendrocyte stem cells were used, this prevented them from becoming oligodendrocytes.
Sim wondered if the opposite effect could also be produced by targeting the same receptor. “So we thought, if we had something that blocks instead of activates this receptor, could we boost differentiation?” Solifenacin, the anti-muscarinic drug for overactive bladder, turned out to be the answer.
“We were excited about this because solifenacin is an approved drug that’s already on the market,” says Sim.
The scientists studied solifenacin’s effects on transplanted human oligodendrocyte progenitor cells in mice that are genetically altered to lack myelin. Remarkably, more oligodendrocytes and myelin resulted from the solifenacin treatment.
With Richard J. Salvi, PhD, SUNY Distinguished Professor in the Department of Communicative Disorders and Sciences, and director of UB’s Center for Hearing and Deafness, Sim also studied whether the induction of oligodendrocytes and myelin created a functional response.
They found improvement in animals with hearing problems that had received transplants with the human oligodendrocyte progenitor cells treated with solifenacin. This was likely due to improvements in neural connections due to extra myelin produced by the oligodendrocytes.
“We have identified a way to improve human myelination,” says Sim. The researchers plan to further study solifenacin in humans.
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