As we each make our way through research journals and publications for our respective interests — mine being multiple sclerosis (MS) — it isn’t uncommon for one of us to find a paper that might be of interest to the other. This week, however, we came across a paper published on February 3, 2020, in Nature Neuroscience that caught the attention of both of us. The word “myelin” — a term likely to be familiar to readers with MS — came up in the title of the piece. Myelin is the insulating sheath around nerves in the brain and spinal cord, and a lack of myelin is the cause of MS symptoms. Those symptoms and their variability have to do with where and how extensively the insulation has been stripped from our nerves.
Too Much or Too Little Myelin May Be a Factor in ASD
The authors of this study seem to have found that over- (and under-) myelination of people with ASD may be a factor in their condition as well. In the case of ASD, the immune system does not strip away existing myelin like it does in MS. According to researchers, oligodendrocytes (the myelin-producing cells) do not seem to produce the correct amount of the fatty insulation. I’ve described the demyelinated nerves of MS as copper telephone cables from which the rubber insulation has been stripped, so that the wire corrodes and signals cannot pass efficiently; in the same way, too much or too little protection may be a factor in ASD. It may also be why the brain volume of people with ASD tends to be either larger or smaller than those of their neurotypical counterparts.
Research May Explain the Range of Symptoms Seen
Just as multiple sclerosis causes a broad range of symptoms, ASD also has a spectrum of impacts. This makes sense to researchers, and even to a layman like myself. For those of us with MS, the more areas affected by demyelination, the more and more severe our symptoms, generally speaking. For people with ASD, too much or two little nerve insulation may create the varied and vast symptoms across the autism cohort.
More Research on Myelin May Benefit Both Diseases
There will be more research needed, and according to a follow-up piece I found, scientists have a plan for that as well. By using tiny clusters of human brain cells called brain organoids, which can be grown in the lab, they hope to discover how and where the myelination problems begin. This could lead to corrective measures to help oligodendrocytes produce the correct amount of myelin. That research, and remyelination research being done in the world of multiple sclerosis, may be co-beneficial to both communities. Caryn and I look forward to continued reporting on this research, and we hope for cross-collaboration between ASD and MS researchers. It’ll give us something to read together. Wishing you and your family the best of health. Cheers, Trevis
