An unlikely drug, already marketed to treat overactive bladder, has triggered the regrowth of myelin in mice.

Researchers from the University at Buffalo have discovered a way to jump start myelin repair using a drug meant to treat overactive bladder.

The breakthrough, announced in a recent study, could pave the way for reversal of nerve damage seen in many neurological conditions, including multiple sclerosis (MS).

A team led by Fraser Sim, Ph.D., assistant professor of pharmacology, discovered that using solifenacin helped cells that make myelin, known as oligodendrocytes, do their job.

In MS, the fatty myelin insulation covering nerves in the spinal cord and brain is destroyed by immune cells. This results in the interruption of signals from the brain to the rest of the body. Symptoms range from mild numbness and tingling to memory loss to balance and mobility problems.

“In MS, myelin is damaged,” Dr. Jack Burks, chief medical officer of the Multiple Sclerosis Association of America (MSAA) told Healthline. The damage “is followed by repair with more myelin producing cells being recruited to the damaged area. Unfortunately, as MS progresses, this repair mechanism is slowed.”

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“Our hypothesis is that in MS, the oligodendrocyte progenitor cells seem to get stuck,” Sim explained in a press release. “When these cells don’t mature properly, they don’t differentiate into myelinating oligodendrocytes.”

A progenitor cell is a step up from a stem cell. It’s already on its way to becoming a specific type of adult cell, but it needs a boost to trigger that action. Sim and his team discovered this final transformation was being blocked. A receptor on the surface of the progenitor cells had been activated and the cells got stuck.

This same receptor is present on the surface of the smooth wall of the bladder. When it’s activated, contractions can occur leading to overactive bladder. The contractions can be controlled with the use of solifenacin, which works by blocking the receptor. This sparked the research team to wonder if the drug could help the stuck progenitor cells, too.

In order to measure how damaged nerves functioned before and after the treatment, Sim teamed up with Richard J. Salvi, Ph.D., director of the Center for Hearing and Deafness at University at Buffalo.

They transplanted human oligodendrocytes treated with solifenacin into hearing-impaired mice unable to grow myelin.

It takes a specific length of time for a signal to pass from the ear, once a sound is heard, to the front part of the brain for processing.

“So in the readout,” said Sim, “you get waves that should have a certain time pattern. When there isn’t enough myelin, the signaling slows down. And if you add myelin, you should see the signals speed up.”

In the mice with transplanted cells, the response time improved.

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It’s still too early to tell if their success with mice will translate to humans, but Sim and his team are determined to find out.

In an interview with Healthline, Sim said his team will be testing their theory in humans soon.

“The planned trial is small and does not require much in the way of external funding,” he said.

It’s too soon to know when the study will get under way. “Without funding in place this is very difficult to precisely say,” Sim added.

For the treated cells to get beyond the tight junctures of the blood-brain barrier and do their job effectively, the stem cells will have to be transplanted in an intracranial procedure. Sim is part of the NYSTEM consortium experimenting with a procedure to implant human cells into MS patients using similar procedures.

This latest development comes during MS Awareness month. Figuring out what triggers MS and how the disease unfolds has been challenging for scientists. Little progress has been made regarding myelin repair, the holy grail of MS research.

Since solifenacin is already FDA approved, if human studies show the same promise as the preclinical experiments, the path to myelin repair could be a short one. The MSAA is cautiously optimistic.

Because this study was only conducted with mice, it’s too early to tell if it will truly repair damage in people with MS, but Burks points out that “other remyelination research projects in MS patient trials are ongoing. For example, anti-Lingo monoclonal antibody therapy is one of the drugs already in clinical trials. The hope for a treatment for remyelination is very promising.”