A new study has discovered a specific gene plays a major role in myelin repair becoming less effective as we age.
To stop MS from getting worse, we need to find ways to repair damaged myelin – the protective coating around nerves in our brains.
Although our bodies have the natural ability to repair myelin, this process breaks down in MS. Recently, researchers have discovered that ageing is a key cause of this breakdown. But they aren’t sure exactly why.
A new study published this week has started unravelling what happens to cause the natural myelin repair process to stop working properly when we get older.
Genes behaving badly
We usually think about genes as the things responsible for characteristics we inherit from our parents, like eye colour. But genes do much more than that. They set in motion all the activities needed to provide our cells with instructions for what they need to do, and when they need to do it.
The study by researchers from the UK, Germany and Italy compared the brains of young and old mice to see which genes were not behaving normally. They found the genes that provide instructions to myelin-making cells were the most affected by ageing.
In particular, a gene called GRP17 played a major role in making myelin repair less effective in the older mouse brain.
Stem cells can’t transition to myelin-making cells
Myelin is repaired or replaced by special cells in the brain called oligodendrocytes. These cells are made from a type of stem cell found in the brain, called oligodendrocyte precursor cells (OPCs).
GRP17 is responsible for instructions to OPCs that are in transition, on their way to becoming fully mature oligodendrocytes. The study found changes in how GRP17 gets those instructions to the OPCs. And this made it harder for the OPCs to turn into oligodendrocytes, which meant myelin repair was less effective.
The researchers also tested a number of molecules that could potentially help older OPCs behave more like young OPCs. One molecule was able to effectively improve myelin repair in older mice.
Potential for new treatments
By uncovering the role of GRP17 in the breakdown of myelin repair as we age, the researchers have identified a potential target for treatments to slow MS progression.
One of the authors, Dr Kasum Azim from the University of Dusseldorf said: “This approach is promising for targeting myelin loss in the aging brain and demyelination diseases, including multiple sclerosis, Alzheimer’s disease and neuropsychiatric disorders. Indeed, we have only touched the tip of the iceberg and future investigation from our research groups aim to bring our findings into human translational settings.”
The interaction between ageing and myelin repair is becoming a hot topic in MS research. Just last week we announced a commitment to raise over a million pounds in funding for research at our Cambridge Centre of Excellence which will include a strong emphasis on understanding myelin repair over the lifespan.
Dr Emma Gray, our Assistant Director of Research, said: “We can see a future where no one has to worry about MS getting worse but, for that to happen, we need to find ways to repair damaged myelin.
"This research sheds light on why cells that drive myelin repair become less efficient as we age, and we’re really proud to have helped fund it. Improving our understanding of ageing brain stem cells could have important implications for future treatment.”