Researchers from the University of Buffalo have found a way to improve remyelination for myelin-based diseases like multiple sclerosis (MS). Results from the preclinical research are published in the Journal of Neuroscience.
Fraser J. Sim, PhD, assistant professor in the Department of Pharmacology and Toxicology in the University at Buffalo School of Medicine and Biomedical Sciences, and colleagues first identified drug candidates that would promote oligodendrocyte differentiation and myelin production. They found differentiation was blocked when muscarinic type 3 receptor on human oligodendrocyte progenitor cells was activated.
By targeting human oligodendrocyte progenitor cells with an antimuscarinic drug, solifenacin, study authors saw a boost in myelination. Solifenacin (marketed as Vesicare) is an FDA-approved drug indicated for patients with overactive bladder with symptoms of urge urinary incontinence, urgency, and frequency.
When human oligodendrocyte progenitor cells were transplanted into mice unable to make myelin, there was an increase in differentiation and myelin synthesis. Using auditory brainstem response as the functional endpoint, Sim and colleagues saw an improvement in the response to auditory signals in animals transplanted with human oligodendrocyte progenitor cells.
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