An MS diagnosis comes with a whole new vocabulary to learn. A host of incomprehensible words can be thrown your way; some trigger vague memories of school biology lessons, some sound like a foreign language, but most are just completely baffling. Suddenly your world is full of nodes, axons and sheaths; experts are talking to you about dendrites and lesions and you may even come across a guy named Charcot. Isn’t he a footballer? (Actually no, he was the doctor widely credited with first identifying MS as a disease, back in 1868.)
One of the words you’re likely to hear pretty often is myelin – often likened to the plastic insulation that covers electrical wires. In much the same way, myelin is a fatty, white substance that surrounds the nerves. The myelin sheath ensures the faster, smoother and most efficient travel of electrical nerve impulses within the central nervous system. Without this protection, not only would your spinal cord need to be the size of a tree trunk (!), but the nerve impulses could misfire into surrounding tissues, meaning that sensory information – like touch or sight – could be delayed or disrupted. When you touch something hot, the normal sensory response is to feel heat, immediately; when myelination is interrupted – as it is in people with MS – the response can be delayed or impaired. Myelin – or rather the destruction of it – has long been linked to the development of MS. Experts agree that myelin is damaged by the autoimmune nature of MS; in other words, the body turns on itself.
Further understanding of autoimmunity and myelin could provide insights into how to treat MS more effectively. It would seem that the academic community agrees with this logic. Scientists are relentlessly seeking solutions as to why myelin becomes damaged in people with MS. The good news is: they’re achieving exciting results. One group of researchers has uncovered a unique phenomenon whereby our usually helpful T-cells (a type of white blood cell critical to the immune system) appear to be instructed to turn rogue by a substance known as interleukin 6 (IL-6). The rogue T-cells subsequently attack and damage the myelin cells, which is thought to be one of the root causes of the myelin plaque development that plagues people with MS.
Further study of immune cells and their influence on myelin destruction has led researchers to discover that the breakdown of myelin itself may initiate a ‘snowball’ autoimmune effect. Myelin breakdown happens in everyone, but it was only when scientists put the spotlight on myelin basic protein (the structural protein of myelin) that they noticed a difference between the way it breaks down in people with MS and the way it breaks down in those without the disease. This discovery suggests that this breakdown of myelin proteins may be the trigger of an autoimmune response.
The mechanisms may be complicated but the results are clear. Without a doubt, maintaining the integrity of myelin is a key concern for everyone involved in MS research. By keeping the focus firmly on myelin, MS researchers will continue to get closer and closer to understanding why the disease is triggered in some people but not others. Maybe one day, we can throw out “multiple sclerosis” from our vocabulary once and for all.