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Image of a mouse brain showing myelin (gold) running through the brain

Researchers discover changing a single gene can boost myelin repair in older mice

Last week, scientists from the MS Society Cambridge Centre for Myelin Repair published new research, adding another piece to the myelin repair puzzle.

Myelin is the protective coating around nerves that gets damaged in MS. When myelin is damaged, the nerve fibres underneath become vulnerable and over time they may be lost. When this happens, messages can’t get through and symptoms become permanent – causing MS progression.

New research shows changing a single gene in mice can make special brain cells, key to myelin repair, more efficient.

What did we already know about OPCs and myelin repair?

Brain cells, called oligodendrocyte precursor cells (OPCs) are responsible for repairing myelin. As we age, our OPCs become less efficient at repairing myelin. OPCs stop responding as well as they should and myelin damage builds up.

Previous research from Cambridge has shown there are ways to make old OPCs behave like younger, more efficient cells. Like giving rats the diabetes drug metformin or growing older OPCs in a soft environment in the lab.

Myc and myelin: What does this research add?

The researchers have discovered a new way to make old OPCs become more ‘youthful’ in mice.

They used genetic engineering techniques to change the level of a single gene, called myc. The researchers increased the activity of myc in older mice, which made the OPCs start behaving like younger cells. This led to better myelin repair. They also altered the activity of myc in young mice and found that the opposite was true: lower levels of myc led to worse myelin repair.

When the scientists looked at why this was happening, they found myc controls the ‘waking up’ process, bringing the OPCs out of a resting state. So they think myelin repair fails when there’s not enough myc to wake up the cell properly.

Will this lead to a myelin repair treatment for MS?

The researchers don’t think we’ll be able to use the same genetic engineering techniques they used in mice, in people with MS. But they hope they’ll be able to target the ‘waking up’ process with drugs.

It might sound like a small step forward, but this discovery that we can improve myelin repair by directly targeting OPCs, rather than changing their environment, is really important.

Dr Bjorn Neumann who led the study said: “Strategies identified so far, including those based on whole-body physiology like fasting, ;change every cell involved in remyelination, not just OPCs. Now we know that you can target the OPC on its own and see an improvement in regeneration, albeit to a smaller degree compared to the whole-body treatments. 

“This challenges the narrative that it’s not possible to improve the function of aged OPCs without direct manipulation of the aged environment. In fact, switching on myc gets you past the ‘bottleneck’ where aged OPCs are unable to successfully contribute to regeneration.”

Professor Robin Franklin, the senior author on the paper, said: “The prospect of changing the age state of OPCs so they can regenerate throughout life is so much better than we’d have thought ten years ago. This is fantastic news for regenerative medicine and chronic demyelinating diseases like MS.”

Dr Clare Walton, our Head of Research said: “We are delighted to have funded this ground-breaking research. MS can be relentless and painful and we know people with MS urgently want us to find treatments that can protect and repair myelin. This latest discovery from Cambridge take us one step closer to that important goal.” 

Read the full study in the journal Nature Ageing

Read about the new trial of metformin in people with relapsing MS