What is multiple sclerosis?
One principle idea I had when setting up this blog was to communicate science and highlight how and in which direction research is done. With this in mind, I also want to explain some brain-related science, so it’s easier to understand what issues are in a specific fields of research. Today I want to start with multiple sclerosis, or short: MS (which is actually the main focus of my PhD project).
MS is a autoimmune disease that affects the central nervous system (short: CNS). Autoimmunity describes the process of your immune system attacking parts of your own body, in case of MS: the CNS. More specifically, your (peripheral) immune cells damage the insulation of your axons called myelin, which can be pictured as the insulation of a electric cable. Axons are necessary to conduct signals from neurons to neurons, or neurons to muscles. When the insulation does not function properly, signals cannot be conducted anymore. Depending on where in the brain the immune system damages the myelin, this can lead to extremely heterogenous symptoms including impairment of vision, tremor, numbness or weakness of limbs, fatigue, and paralysis.
MS can develop in genetically susceptible individuals, but the environment seems to play a bigger role. By environment I mean factors such as smoking, infections, or vitamin D deficiency. In fact though, we actually have no idea what the cause of MS is. There are even voices suggesting that MS is not (primarily) an autoimmune disease. It has been difficult to pinpoint a specific cause of MS because there is not one specific cause. More likely, multiple factors have to line up in a particular way in order for MS to develop. Hence, it is difficult to study the cause of this disease. Good news is, however, that we can still study it’s pathophysiology and come up with treatments (but not cures so far!).
Most current MS treatments target the immune system and aim to reduce it’s activity. The effectiveness of these treatments again underscores the notion that MS is an autoimmune disease. However, as MS progresses to more advanced disease, these treatments are often not effective anymore. Reasons for this are that the immune system does not seem to play a major role in advanced disease anymore, but that the disease progresses from the inside of the CNS. As the myelin layers get damaged, neurons will eventually die; a process called neurodegeneration. Furthermore, the cells creating these myelin layers, namely oligodendrocytes, are dying as well. Altogether, this process can activate a brain-internal cascade of events that leads to a progression of disease without involvement of the (peripheral) immune system.
In order to interfer with this process, research now focuses on what factors influence disease progression in later stages. For example, it will be important to study how to promote the remyelination of the axons once the immune system is “cooling-off” and thereby avoiding excessive neuronal death, and restore functionality.
As so often in science, we will probably need many more years to understand exactly how MS progresses and how we can interfere. Along the way, we might actually find out what the cause is of MS. What’s for sure is that our knowledge is expanding, so we are getting closer every year.
