This week I decided to look deeper into remyelination. As mentioned in last week’s post, patients with MS experience demyelination. Their immune system attacks the myelin sheaths on their nerve fibers, which are needed to transmit signals from the brain. Other than the death of oligodendrocytes, a cause of demyelination is the “robust immune responses mediated by microglia, which are the resident immune cells of the central nervous system.” (multiplesclerosisnewstoday) Recent studies show that microglia may actually be beneficial in promoting remyelination by promoting regeneration and clearing myelin debris.
“Aiming to better understand the role of microglia in MS, scientists at Université Laval, in Canada, administered a molecule called macrophage colony-stimulating factor (mCSF) to mice receiving dietary cuprizone.” (multiplesclerosisnewstoday) The mCSF shifted the microglia to become anti-inflammatory, promoting remyelination. This research suggests that “mCSF would be an ideal target for a clinical trial in individuals diagnosed with primary and secondary progressive MS.”
Immune Response Promotes Remyelination in MS Mouse Model
Multiple sclerosis is an autoimmune disease that affects 2.3 million people worldwide. The immune system attacks the central nervous system, which consists of the brain and spinal cord. With MS, the immune system causes damage to the myelin that surrounds and insulates the nerve fibers. When the myelin and nerve fibers are damaged, they stop sending signals from the CNS to the brain, and the damaged areas develop scar tissue. This gives it the name multiple sclerosis – multiple scarring.
While MS cannot be cured, it can be treated. One of the more recent breakthroughs for this disease is remyelination – the spontaneous regeneration of the myelin that surrounds and insulates nerve fibers. Researchers at the University of Buffalo have found that drug targeting a receptor called muscarinic type 3 (M3R), found on OPC cells (the cells that make myelin), works to help remyelination. In people with MS, the activation of M3R prevents OPC cells from maturing properly. Using a drug already on the market for overactive bladders (solifenacin), scientists have successfully inhibited M3R, letting the OPC cells work to repair myelin.
This recent research establishes that once M3R is blocked, remyelination becomes possible. It also helps us understand the role of receptors in autoimmune diseases like MS.