Paul: Why is remyelination slower in MS?
Dr Dave Lyons, Researcher: Okay, that’s a great question. I mean, one thing to bear in mind is that there’s good news that we actually have the cells that can repair myelin in our nervous systems. So about five per cent of the cells in our adult central nervous system, our brain and spinal cord, are so-called oligodendrocyte precursor cells. Now these are the cells that generate myelinating oligodendrocytes when we’re young and throughout life. So these cells are present and able to repair damaged myelin. So if there is damage to myelin, the oligodendrocyte precursor cell has to recognise that there’s damage. It may often have to migrate to move to the site of damage, it may have to divide and multiply so that there are sufficient cells to repair the damage, and then there’s the issue of that cell then has to start moving and searching around, but actually differentiate, so take on a different sort of behaviour altogether where it looks for and interacts with axons that it wraps myelin sheets around. So in MS we know that about 30% of lesions, there’s actually a failure of these cells to reach the lesion, and this could again be due to the fact that there is problems in their migration to the lesion or perhaps they can’t even get past some barrier of the lesion to undergo remyelination. However, in about 70% of lesions the oligodendrocyte precursor cells are there, but they seem to fail to differentiate into the myelin producing oligodendrocytes. So that’s why we as a research community think that pushing these oligodendrocyte precursor cells to differentiate more and better and faster is an important goal for the treatment of MS, because this seems to be a block, a bottleneck during multiple sclerosis that explains some of the reasons for slow remyelination.
Paul: That’s very interesting. And at the same time it seems to be a very complex process. Are there any other approaches that could speed up this remyelination process?
Dr Dave Lyons: Yeah, absolutely. So I mean of course lesions are different in different people at different times, so in some cases you may want to actually accelerate the cell’s ability to get to a lesion. Now of course a lesion isn’t simply oligodendrocytes and axons, but there are various other cell types, like cells of the immune system that will regulate the environment that need to be modulated and can be modulated as well to sort of improve myelin repair.
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Dr David Lyons received his PhD from from University College London in 2003. Dr Lyons has been with the centre for neuroregeneration since 2009 through a BBSRC fellowship. Dr Lyons received a Research Prize from the Lister institute in 2012 and a senior research fellowship from the welcome trust in 2014.