Remyelination and Multiple Sclerosis
Written by Lillian Brinkmann
Edited by Sameeha Salman
March 21, 2022
Edited by Sameeha Salman
March 21, 2022
Have you ever noticed the outer layer of insulation on wires and cables? The purpose of this layer is to help conduct electrical currents quickly and efficiently. As it turns out, we have something similar in our own brain cells! A pivotal foundation of our bodily functions is the electrical impulses that run through our nervous system, which do everything from allowing us to feel sensations to letting us move our muscles. These currents travel along cells called neurons, which have long, noodle-like projections called axons. Axons are wrapped in a layer of special cells called myelin, which, similar to any cable you may have in your home, provides insulation to help move those electrical signals along. But what happens when myelin is gone?
As relayed in this article from Journal of Neurology, the disease multiple sclerosis (MS) causes the immune system to mistakenly attack myelin, destroying that crucial electrical insulation. Without myelin, those important electrical currents will not move as efficiently or swiftly, causing symptoms like “weakness, sensory loss, and diplopia (double vision)”, as well as difficulty swallowing, loss of coordination, and more. This debilitating disease affects many, so how can we treat it? While there are drugs to relieve symptoms, like Adderall, Botox, or Zoloft, some researchers have directed their attention to eliminating MS via remyelination, the process by which myelin is rebuilt along the axon.
To understand possible treatments for remyelination in MS, we must understand where myelin comes from in the first place. As we develop, cells called oligodendrocytes create the myelin sheath. If the sheath is damaged in adults, a special type of oligodendrocyte, adult oligodendrocyte progenitor cells (aOPCs), mediate the creation of new myelin. Unfortunately, the act of creating aOPCs and employing them to rebuild myelin is a multi-step process that has plentiful room for error. For example, debris from destroyed myelin contains signals that prevent the creation of aOPCs. Age and time also play a factor, with studies suggesting that remyelination is inhibited in patients over age 55 and in those who have had MS for over 10 years.
Treatments for remyelination need to take many factors into account to ensure success. One potential treatment is clemastine, an antihistamine that may promote the creation of aOPCs. Another treatment could utilize an antibody called opicinimab, which has been shown to promote remyelination by inhibiting Lingo-1, a compound that hinders oligodendrocyte function. We can measure the efficacy of these treatments using procedures like MRIs and magnetisation transfer techniques, which both quantitatively demonstrate the extent of remyelination. For a qualitative measure, we can assess patients based on improvement of symptoms, such as through sensory, auditory, or motor exams.
Overall, remyelination is a complicated process that necessitates more studies to be fully understood. Factors like potential remyelination failure, what treatments are most efficient, and when exactly those treatments should be employed must be further explored. However, researchers have made headway in understanding these mechanics, such that we have hope for the future of MS treatment. With all the studies and trials currently taking place, it’s clear that our neurons’ electrical insulation is in good hands.
Image Source: “Stem cell diagram on white background Free Vector” by Brgfx licensed under Freepik License