One of the key changes that occurs in the brain and spinal cord in MS is patchy damage to myelin (plaques). Myelin is the fatty coating that helps nerves to pass signals from one part of the brain to another rapidly and without loss of signal. In the relapse remitting phase of MS new symptoms may appear or established symptoms may worsen. It is believed that changes in symptoms during a relapse can be attributed to newly formed plaques or to older plaques being reactivated. Repeated relapses are associated with gradually developing brain and spinal cord damage over time and this is reflected in a new or worsening symptom profiles. Relapses are associated with inflammation which affects brain function and structure. Steroids to reduce the level of inflammation are generally prescribed during a relapse. In recent years, the focus of research on reducing the number and severity of relapses has led to several new drugs that have successfully reduced the number of MS relapses experienced in the early relapse remitting phase of MS. Less attention has been given to why remyelination does not occur successfully to restore function in MS after an attack. Despite the presence of immature oligodendrocytes (the cells that make myelin) in plaque areas of the brain and spinal cord these cells do not progress to adult oligodendrocytes able to produce new and effective myelin. It follows then that one very important problem to solve in MS is to understand what stops repair to myelin damage.
The process of myelin formation in the developing nervous stem is extensively studied in several laboratories world-wide seeking to understand the myelination process more fully. More importantly for MS, researchers are also trying to understand what prevents remyelination in areas of MS related damage. In a recent study entitled “Regulatory T cells promote myelin regeneration in the central nervous system” researchers from laboratories across the UK, the wider European community, and the USA have joined forces to try and unravel the reasons for myelin regeneration failure in MS and other conditions. This is an important example of how international research engaging people with detailed knowledge of MS, new technologies to help understand cellular processes and in depth knowledge of myelin formation have come together to address this question in MS.
The study, using a mouse model of demyelination like that occurring in MS, suggests that we need to understand much more about the environment in which attempted remyelination takes place. Particularly they report that remyelination requires the activity of a specific immune cell that they call T reg. -a regulatory T lymphocyte. In complex studies, they removed the influence of the T reg. cells and then replaced them. Removing the cells resulted in poor myelin regeneration while replacing them resulted in much improved remyelination. This type of study is carried out in tissue maintained outside the body and may not translate directly to how the interaction between cells works in the body. Further it cannot be assumed that the same process will work if applied in human subjects. Never the less it is a very important step in understanding what we may need to know before we can promote good remyelination in people who have MS.