Neuron: Scientists have developed new ways to restore myelin function in damaged nerve cells or hopefully help treat multiple sclerosis

November 16, 2020 // -- The absence of myelin is one of the reasons nerve cells are unable to recover after injury and certain diseases, myelin is a lipid material encased around the axons of nerve cells, which, like insulators, covers longer axons, making high-speed communication between neurons possible, without myelin, neurons may not be able to communicate better, thus making it impossible to perform the desired function.
In a recent study published in the international journal Neuron, scientists from Boston Children's Hospital and others found a two-pronged approach that restores myelin on regenerative axons in models of optic nerve-damaged mice, and the findings are important for treating myelin deficiency-related diseases such as multiple sclerosis. Zhigang He, a researcher at
, said the study may be an important step toward restoring cellular function in the central nervous system in adults. In earlier studies, researchers have found that multiple therapies promote the regeneration of damaged axons in the optic nerve, but fail to restore nerve function, so what is the reason? These regenerative axons cannot be myelin, and in this study, the researchers explain why these axons cannot be re-myelinized after injury.
in the adult brain, myelination is done by less protrusive glial cells (OPCs, olgodendrocyte precursor cells).
Photo Source: Wikipedia researchers point out that OPCs do not differentiate into mature, myelin-forming, less protrusive glial cells in damaged optic nerves, meaning they do not develop into cells capable of producing myelin and functioning properly; This phenomenon can be explained by the fact that OPCs in the damaged nerve can elobody a special protein called GPR-17, thus blocking the first stage of OPC differentiation into mature cells, and secondly, the inflammatory cells in the damaged nerve interfere with another stage of OPC differentiation.
When a range of available compounds were tested, the researchers found that montelukast, an anti-inflammatory drug used to treat asthma and seasonal allergies, could block the function of GPR-17, and that the myelin regeneration process of some axons could be restored, but only in about 15 percent of the nerve cells treated.
When small glial cells are removed from damaged nerve cells using a drug called PLX3397, myelin formation increases significantly, and PLX3397 increases the myelin regeneration process by 21%, and when used in combination with Monrust, this combination therapy may allow about 60% of damaged axons to have myelin regeneration.
Small glial cells may act as "scavengers" in the body's central nervous system, looking for damaged inflammatory cells and infectious compounds and removing them from the damaged site, however, in this case, the presence of small glial cells may also block OPCs from developing into normal less protrusive glial cells, and after further studies of small glial cells, the researchers noted that opC development becomes normal when small glial cells are removed after damage to the body (two weeks after nerve damage).
researcher He points out that in mouse models of optic nerve damage, we found that most axons may have myelin regeneration when combined with therapy to remove small glial cells after damage to the body.
In the late stages of multiple sclerosis, damaged nerve tissue suffers from the failure of the myelin regeneration process, as this study was not conducted in mouse models of multiple sclerosis, but in fact researchers have found a way to make the regenerative axon myelin regeneration process, which is important for researchers, as there is currently no available multiple sclerosis therapy to play a therapeutic role by reconstructing myelin.
Finally, the researchers say this is similar to what we observed in the optic nerve after the injury, and when myelin failure is suffered, we believe that the results of this paper may be of great clinical significance for the development of new types of multiple sclerosis therapies, especially those with advanced multiple sclerosis.
() Original source: Jing Wang, Xuelian He, Huyan Meng, et al. Robust Myelination of Regenerated Axons Induced by Combined Devices of GPR17 and Microglia, Neuron (2020). DOI: 10.1016/j.neuron.2020.09.016