CRM supports #StopMS campaign

CRM group leader Anna Williams has lent her support to the MS Society’s Stop MS campaign with an interview featured on the BBC News at Six.

On the 8th of October the MS Society’s Stop MS Appeal went live to the public. It aims to raise £100 million over the next 10 years in order to spur on the research going into treatments for multiple sclerosis, a neurodegenerative disease which affects more than 100 000 people in the UK alone. 

Anna Williams, Professor of Regenerative Neurology at the University of Edinburgh, was featured in the BBC News at Six alongside the announcement of the Stop MS Appeal launch because of her team’s ground-breaking research into the mechanisms by which the nerve-protecting myelin sheath becomes damaged during MS, and what can be done to stimulate its repair. 

As she told BBC correspondent Caroline Wyatt:

“At the moment, with progressive forms of MS, we can always give relief for pain or stiffness but we won't change the course of the disease. So for those patients, to slow or stop or reverse the disease can only be done with more research, and money is critical for research.”

Professor Williams was part of the international collaboration which showed for the first time that humans, like mice, have multiple forms of myelin-repairing cells called oligodendrocytes in the brain. The research which stemmed from this collaboration, published in Nature earlier this year, also showed that the proportion of these different kinds of oligodendrocytes is different in people with MS compared to people not suffering from the condition. 

Her team is focused on trying to understand why these cells, which should be constantly repairing any damage inflicted upon our nerves’ protective myelin sheath, stop working. Normally, these cells should be attracted to areas of damage, and through a number of processes build the myelin back up. The fact that there are multiple processes means that there are a number of points at which the repair could be going wrong, and understanding how all the different mechanisms should work could be key to understanding how to fix them. 

By investigating what molecules prevent the attraction of oligodendrocytes to areas of myelin that need repairing, and what drugs are effective in stopping these molecules from signalling, Professor Williams and her team hope to find a way to allow the normal repair of myelin to resume in people suffering from MS. 

As she told the MS Society this month:

“Myelin repair will be a key part of how we treat MS for everyone in the future. You can't put myelin back onto nerves that have already been lost. So myelin repair won't reverse disability for people with advanced progressive MS. But it could be hugely beneficial in slowing or stopping progressive MS.”

Article written by Laura Marenco