In a study published in the journal Nature Communications, researchers have found out that a particular type of cell is much more prolific in generating a protective sheath covering nerve fibers than previously thought. When they got the revelation about Schwann cells, it raises the possibility of new avenues to treat nerve injuries and various forms of neuropathy. Additional research could prove useful in promoting myelin repair in central nervous system disorders such as multiple sclerosis, where damage to myelin slows or blocks electric signals from the brain.
As the senior author of the study, Kelly Monk, Ph.D., professor, and co-director of the Vollum Institute at Oregon Health & Science University, said, this discovery overturns the textbook definition of the way Schwann cells work.
The two types of cells in the body that produces myelin are oligodendrocytes in the brain and spinal cord, and Schwann cells in the rest of the body. Until recently, scientists believed that only oligodendrocytes generated multiple myelin sheaths around axons, the slender projection of a nerve cell that carries electrical signals between cells. In the new research, the team found out that Schwann cells are also capable of spreading myelin across multiple axons.
The team found out about this after they conducted a genetic screen in zebrafish in the Monk laboratory. They identified some fish had more myelin than expected, and those fish carried a mutation in a gene calls fbxw7. When they knocked out the gene in genetically modified mice, they discovered an unexpected characteristic such as individual Schwann cells began spreading myelin across many axons. According to Monk, it highlights a very plastic potential for these cells.
In evolutionary history, both Schwann cells and oligodendrocytes arose at the same point, with the appearance of jaws in the vertebrate lineage. Invertebrates lack myelin, and some like the modern squid uses thick axons to transmit signals between neurons quickly. Monk noted that they could have evolved that way, but their spinal cord would be the diameter of a giant sequoia tree.
By contrast, remyelination in the central nervous system tended to be an evolutionary dead end since few would have survived a severe whack to the brain or spine. Monk explained that there's no selective pressure in repairing myelin damage in the central nervous system because you are probably going to die. However, the discovery the researchers published suggests a new opportunity to heal the brain and spine. Monk concluded that targeting the fbxw7 gene, or downstream pathway molecules, could be a powerful way to promote myelin repair in the central nervous system.
