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The Express Gazette
Sunday, February 22, 2026

Hope for MS sufferers as drug combo shows potential to repair nerve damage

Cambridge trial suggests metformin and clemastine may preserve nerve signaling in relapsing MS; long-term safety and effectiveness await further study.

Health 5 months ago
Hope for MS sufferers as drug combo shows potential to repair nerve damage

Researchers say they are on the brink of a breakthrough treatment for multiple sclerosis that could repair nerve damage by rebuilding myelin, the protective sheath surrounding nerve fibers. MS occurs when the body targets myelin, leading to a range of debilitating symptoms such as fatigue, pain, muscle spasms and problems with walking. In recent work, scientists have tested a combination of metformin, a widely used diabetes drug, and clemastine, an antihistamine, and found that the pair may help repair myelin and potentially slow disease progression. Repairing the myelin membrane could also help protect damaged nerves from further degeneration and restore some neural function.

In the Cambridge Centre for Myelin Repair Two trial, 70 participants with relapsing MS took part over six months. Half received the drug combination and half received a placebo. Researchers assessed the speed at which visual signals travel from the eye to the brain, a proxy for overall nerve conduction. The results indicated that while signal speed declined in the placebo group over the six-month period, it remained stable in the group receiving metformin and clemastine, suggesting a preservation or partial restoration of nerve function. The researchers said the findings warrant publication in a peer‑reviewed journal and emphasize that longer studies are needed to determine how durable these effects are and whether any adverse effects emerge with extended use.

Dr Nick Cunniffe, an academic neurologist at Cambridge University who led the trial, cautioned that scientists still need to study the long-term benefits and potential side effects before the regimen could be considered by people living with MS. “We still need to research the long-term benefits and side-effects before people with MS consider taking these drugs,” he said. “But my instinct is that we are on the brink of a new class of treatments to stop MS progression, and within the next decade we could see the first licensed treatment that repairs myelin and improves the lives of people living with MS.” The study, which built on prior animal research showing metformin enhances the effect of clemastine, marks a milestone in pursuing therapies aimed at repairing the nerve sheath rather than merely modulating immune activity.

The research was supported by the MS Society, which funds investigations into myelin repair and related therapies. Dr Emma Gray, director of research at the MS Society, described the results as a potential turning point. “These results could represent a turning point. This research gives us real hope that myelin repair drugs will be part of the armoury of MS treatments in the future,” she said. More than 150,000 people in the United Kingdom live with MS, a figure that underscores the potential impact of therapies capable of repairing damaged myelin. While the combination had shown promise in prior animal studies, this is among the first human tests to examine whether restoring the myelin membrane can translate into measurable improvements in nerve signaling and, by extension, functional outcomes for patients. Additional work is needed to clarify dosing, safety profiles, and which patients might benefit most, particularly given the varied courses MS can take from person to person.

If future trials corroborate these early signals, researchers anticipate integrating myelin repair strategies with existing disease-modifying therapies to form a broader approach to MS management. The path from early promise to an approved treatment, however, remains lengthy and uncertain, requiring larger, longer trials to assess sustained efficacy and safety across diverse populations. In the meantime, the current findings contribute important evidence that rebuilding myelin could become a viable therapeutic goal rather than a distant aspiration, offering renewed hope to patients, families and clinicians navigating this complex neurological disease.


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