U of M researchers battle MS from new angle

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This article was published 22/05/2018 (3057 days ago), so information in it may no longer be current.

It’s potentially game-changing research that’s going on in our backyard.

And it’s sorely needed in the battle against multiple sclerosis — perhaps here in Manitoba more than anywhere else.

Manitoba has among the highest rates in the world of the MS — a disease in which the immune system attacks the nervous system for reasons that largely remain a mystery.

Homegrown work by one of the nation’s leading MS investigators aims to create a new form of treatment that could significantly slow down the disease — if not stop it in its tracks.

“We know that multiple sclerosis destroys the myelin sheath — a fatty protective layer that surrounds the nerve fibre,” says Dr. Soheila Karimi, who heads the Karimi Laboratory, a research program for spinal cord injury, multiple sclerosis and regenerative medicine at the University of Manitoba.

While current treatments are effective in reducing the body’s erroneous immune system response toward nerve tissue, her research team’s work involves a different approach.

“Most of the treatment options available tackle inflammation to reduce the impact of these attacks — the autoimmune attacks on the myelin sheath,” says Karimi, an associate professor in the Max Rady College of Medicine at the University of Manitoba.

So while available medication reduces injury to the nervous system, it does not repair the damage.

“But our research aims to actually repair the myelin that is gone around the nerve fibre.”

If successful, her work would represent a turning point in treating MS.

Karimi’s team isn’t alone in its quest to reverse the disease’s damaging effects, says Darell Hominuk, director of government relations and stakeholder development for the Manitoba division of the MS Society of Canada.

It is among several studies supported by donations from Canadians to the MS Society, “dedicated to finding answers about myelin repair,” he says.

“Our goal is to invest in research that will provide the greatest benefit to individuals who are affected by MS.”

With May being MS Awareness Month in Canada, with World MS Day taking place May 31, donations from Canadians are critical to advancing this kind of research, he adds.

What’s more is the work of scientists and medical doctors in Manitoba is often at the leading edge of the investigation into MS, Hominuk says.

That’s why the Free Press is showcasing, in this article and another on May 28, some of the pioneering work taking place in the province aimed at improving the lives of the thousands of Manitobans and Canadians with the disease.

Karimi’s research, focused on repurposing drugs used for treating other illnesses to fight MS, is indeed among the most compelling. Her team has already demonstrated positive results in promoting myelin repair in animals.

Those findings will likely be published in the next year or so, but she recently spoke with the Free Press to offer readers insight into what’s gone on in her lab so far.

“We are trying to understand how remyelination happens, its processes and what factors regulate these processes,” she says.

“Then we want to know how we can, through treatment, boost the process of remyelination so we can accelerate recovery and promote the regeneration of neural tissue.”

Karimi likens the myelin sheath to the plastic coating on an electrical cable. Basically, it acts as insulation allowing the signal from the nerve cell to pass along the axon, which is a fibrous extension of the neural cell — much like an electrical cord.

When the sheath is damaged, the signal degrades and impairs bodily function. The effects can be wide-ranging, from dizziness, tingling and numbness to difficulty walking and vision impairment.

Equally important, the sheath protects the nerve fibre from damage and permanent loss of function.

With MS, the immune system turns on the body, targeting cells — called oligodendrocytes — found in the brain and spinal cord that regenerate the myelin sheath.

“And it’s the death of oligodendrocytes that causes myelin damage around nerve fibres resulting in functional impairment,” Karimi says.

At first, most people with MS have mild symptoms because the regeneration of myelin still occurs, albeit at a slower pace.

That’s why most MS patients experience remitting and relapsing illness with periods of symptoms and disability followed by spans of being largely symptom-free.

Current treatments help slow the disease by reducing damage to the cells, making it easier for the body’s normal mechanism to repair the damage. But myelin regeneration is slow and becomes increasingly impaired over time for people with MS.

“This capacity (to regenerate) declines because over time those cells making new myelin are gone.”

Moreover, the nerve fibres are left exposed more and more, leaving them susceptible to damage, which becomes permanent.

Consequently, many patients’ disease becomes progressive, with no remission of symptoms.

Yet even when the myelin sheath is repaired normally, the coating is thinner than before.

“So we don’t just want to promote remyelination; we also need to promote the quality of remyelination,” she says.

As previously mentioned, Karimi and her research team are examining already-approved drugs for other non-MS treatments that may promote and accelerate myelin regeneration.

These medications can be fast-tracked to clinical use, given their safety is already largely established.

While Karimi cannot discuss what drugs her team is working with, due to issues relating to patents, she says these therapies target progenitor cellsfound in the brain and spinal cord that can be recruited to replace mature oligodendrocytes that renew the myelin.

“We want to activate those cells and increase their numbers, so they can replace myelin endogenously (produced within the body).”

She adds this is a different technique than stem-cell therapies her lab is also exploring for spinal cord injury therapeutics.

While stem cell therapies could spark regeneration, they would be a bandage approach to MS, which often involves widespread lesions.

In contrast, treatments that recruit the body’s own cells to replace the damaged cells throughout the nervous system would be much more effective, Karimi notes.

If her work proves fruitful, it could lead to a new class of drugs used alongside current treatments.

“We have good medications that control the immune system response and limit damage, but we also need to repair the damage,” Karimi says.

“And that’s our goal.”

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