March 23, 2020, by mstalniceanu

Myelin: An unknown saviour for the brain

By Sakaorna Jeyanathan 

During my final year of my degree in neuroscience, I have delved into the function of myelin in a lot of detail¹. Myelin is an important membrane structure of the brain which is made from fats and acts as an insulating and protective layer for neurones². It also increases the speed of transmission of electrical impulses (called action potentials) which are formed by the movement of sodium and potassium ions³. In the brain and spinal cord, cells called oligodendrocytes produce and wrap myelin around axons of the neuron⁴. The membranes provide a thick layer which is impermeable the ions mentioned above¹. This helps action potentials to be carried in one direction and increases the conduction of the action potential as they can undergo saltatory conduction¹. Unmyelinated neurones also exist but these are for slower responses such as digestion². The breakdown of this lipid membrane can cause consequences to neuronal function. This is called demyelination and has been observed in many disorders². When the myelin is lost, the action potentials are slower which could lead to the damage of nerve fibres².

The causes of demyelination are²:

• Inflammation- usually when your body is co-ordinated to attack its own cells (autoimmunity)
• Loss of oxygen to the brain – hypoxic-ischemic demyelination
• Focal compression
• Virus’ (JC virus)

Multiple sclerosis (MS) in particular is a common disorder that causes demyelination. It is a debilitating disorder that affects around 2 1/2 million worldwide⁵. This disorder is termed an autoimmune disorder, when the body’s immune system begins to attack the body⁶. However, it is organ specific; the disorder only affects the brain and spinal cord⁷. One of the consequences of this is that the myelin sheaths can disintegrate. Not only this, but the cells producing myelin (oligodendrocytes and Schwann cells) can also be damaged⁷. In turn this can cause the reduction in the speed of firing of neurons, which can be critical for certain neurones which are required to transmit information at a higher speed⁷. This effect is widespread throughout the nervous system and can impact numerous daily tasks. One of the main effects of this is that this can lower the ability to coordinate movement and therefore reduce the function of the muscles⁷. This can also result in the loss of myelin for axons that are part of vast neural networks necessary in regulating functions such as cognition⁸. Patients with MS can have difficulties with their working memory (short term memory and memory related decision making)⁸.

Indeed, the brain can undergo a process called remyelination⁹. This is a process which is triggered by demyelination. Cells called neural progenitor cells can newly form and move to the area of demyelination and turn into cells that produce oligodendrocytes. However, these cells⁹. However, in patients with MS, these new cells only produce thinner myelin sheaths and are shorter in length⁹. These do not fully cover the neuron’s axon and can still reduction the speed of transmission⁹.

Currently, scientists are attempting to increase the efficiency of remyelination in MS patients are current treatment (immunomodulators) do not aid the improvement of remyelination⁹. Current therapies that have been theorised is cell induced therapy which is to inject stems into areas of the brain with less myelin⁹. This has been conducted in mouse models, but it is easier said than done⁹. Much research is current ongoing to test this theory and if this method is successful, this can definitely change the lives of many MS patients⁹.

References

1. Fields, R. D. Myelin – More than insulation. Science (80-. ). 344, 264–266 (2014).
2. Nave, K.-A. & Werner, H. B. Myelination of the Nervous System: Mechanisms and Functions. Annu. Rev. Cell Dev. Biol. 30, 503–533 (2014).
3. Morell, P. & Quarles, R. H. Characteristic composition of myelin. Basic Neurochem. Princ. Mol. Cell. Med. Neurobiol. 1096 (2012).
4. Bradl, M. & Lassmann, H. Oligodendrocytes: Biology and pathology. Acta Neuropathol. 119, 37–53 (2010).
5. Multiple sclerosis society. MS in the UK. 3 (2016).
6. Martin, R., Lutterotti, A. & Martin, R. and Lutterotti, A. Molecular Basis of Multiple Sclerosis: The Immune System. (2010).
7. Chen, M., Gran, B., Costello, K., Johnson, K. & Martin, R. Multiple Sclerosis. 168–171 (2001). doi:10.1177/135245850100700401
8. Karavasilis, E. et al. Hippocampal structural and functional integrity in multiple sclerosis patients with or without memory impairment: a multimodal neuroimaging study. Brain Imaging Behav. 13, 1049–1059 (2019).
9. Olsen, J. A. & Akirav, E. M. Remyelination in multiple sclerosis: Cellular mechanisms and novel therapeutic approaches. Journal of Neuroscience Research 93, 687–696 (2015).

Photo by Colin Behrens from Pixabay

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