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The quest to repair the damage caused by multiple sclerosis is gaining momentum, with scientists working to restore lost function and slow progression by rebuilding myelin—the protective coating of nerve cells. Within the brain and spinal cord, immature myelin-making cells called OPCs hold promise, but need the right signals to mature into oligodendrocytes and repair MS lesions. Researchers are also studying the role of microglia, the immune cells that clear debris but can turn destructive, with drugs like BTK inhibitors potentially tilting them toward repair.
Early attempts at remyelination drugs such as opicinumab and elezanumab showed promise in animals but ultimately failed in human trials, underscoring the challenge. Still, reasons for optimism are emerging: clemastine, a common antihistamine, showed signs of remyelination in optic neuritis, while PIPE-307—a compound inspired by green mamba snake venom—is in Phase 2 trials. Even novel approaches like gold nanoparticles are being studied to boost oligodendrocyte energy and repair capacity. The path is complex, but progress is accelerating—bringing remyelination therapies closer to becoming a real option for people living with MS.
Barry Singer MD, Director of The MS Center for Innovations in Care, interviews:
Veronique Miron PhD, MS Research Chair at St. Michael's Hospital and Professor of Immunology at The University of Toronto
Robert Glanzman MD, Board-certified neurologist and Chief Medical Officer of Find Therapeutics
By Barry Singer, MD4.9
119119 ratings
The quest to repair the damage caused by multiple sclerosis is gaining momentum, with scientists working to restore lost function and slow progression by rebuilding myelin—the protective coating of nerve cells. Within the brain and spinal cord, immature myelin-making cells called OPCs hold promise, but need the right signals to mature into oligodendrocytes and repair MS lesions. Researchers are also studying the role of microglia, the immune cells that clear debris but can turn destructive, with drugs like BTK inhibitors potentially tilting them toward repair.
Early attempts at remyelination drugs such as opicinumab and elezanumab showed promise in animals but ultimately failed in human trials, underscoring the challenge. Still, reasons for optimism are emerging: clemastine, a common antihistamine, showed signs of remyelination in optic neuritis, while PIPE-307—a compound inspired by green mamba snake venom—is in Phase 2 trials. Even novel approaches like gold nanoparticles are being studied to boost oligodendrocyte energy and repair capacity. The path is complex, but progress is accelerating—bringing remyelination therapies closer to becoming a real option for people living with MS.
Barry Singer MD, Director of The MS Center for Innovations in Care, interviews:
Veronique Miron PhD, MS Research Chair at St. Michael's Hospital and Professor of Immunology at The University of Toronto
Robert Glanzman MD, Board-certified neurologist and Chief Medical Officer of Find Therapeutics

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