Myelin & Multiple Sclerosis | Living Like You
Myelin under the microscope

A Multiple Sclerosis (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

What is Myelin?

One of the words you’re likely to hear pretty often is myelin. Myelin is often likened to the plastic insulation that covers electrical wires because, in much the same way, myelin is a fatty1, white substance that surrounds the nerves. The myelin sheath ensures fast, smooth and 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. Experts agree that myelin is damaged by the autoimmune nature of MS; in other words, the body turns on itself2.

How can Myelin help?

Further understanding of autoimmunity and myelin could provide insights into how to treat MS more effectively. Scientists are seeking and achieving solutions as to why myelin becomes damaged in people with MS. 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) 3. The rogue T-cells subsequently attack and damage the myelin cells, causing de-myelination4.

Further study 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 disease5. This discovery suggests that this breakdown of myelin proteins may be the trigger of an autoimmune response5.

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.

References:

  1. Morell P, Quarles RH. The Myelin Sheath. In: Siegel GJ, Agranoff BW, Albers RW, et al., editors. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Philadelphia: Lippincott-Raven. 1999. Available from: https://www.ncbi.nlm.nih.gov/books/NBK27954
  2. Duncan ID, Radcliff AB. Inherited and acquired disorders of myelin: The underlying myelin pathology. Exp Neurol. 2016 Sep;283(Pt B):452-75. doi:10.1016/j.expneurol.2016.04.002. Epub 2016 Apr 9.
  3. Heink S. et al. Trans-presentation of IL-6 by dendritic cells is required for the priming of pathogenic TH17 cells. Nat Immunol. 2017 Jan;18(1):74-85. doi: 10.1038/ni.3632. Epub 2016 Nov 28.
  4. Ignatius Arokia Doss PM, Roy A-P, Wang A, Anderson AC, Rangachari M. The Non-Obese Diabetic Mouse Strain as a Model to Study CD8+ T Cell Function in Relapsing and Progressive Multiple Sclerosis. Frontiers in Immunology. 2015;6:541. doi:10.3389/fimmu.2015.00541.
  5. Friedrich MG, Hancock SE, Raftery MJ, Truscott R. Isoaspartic acid is present at specific sites in myelin basic protein from multiple sclerosis patients: could this represent a trigger for disease onset? Acta Neuropathol Commun. 2016 Aug 12;4(1):83. doi: 10.1186/s40478-016-0348-x.

 

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