Activation of the immune response mediated by cells called microglia favors remyelination and myelin repair in multiple sclerosis (MS), according to a new Canadian study using mice.
The research, “mCSF-Induced Microglial Activation Prevents Myelin Loss and Promotes Its Repair in a Mouse Model of Multiple Sclerosis,” was published in the journal Frontiers in Cellular Neuroscience.
MS patients typically present progressive demyelination, or loss of myelin (the protective layer of nerve fibers), which leads to impaired nerve transmission. Although remyelination (the formation of new myelin) occurs spontaneously in MS lesions, it becomes increasingly incomplete and eventually fails.
Among the factors involved in demyelination in these patients are the death of oligodendrocytes — cells producing myelin — and robust immune responses mediated by microglia, which are the resident immune cells of the central nervous system.
However, an increasing number of studies suggest that microglia may be beneficial in disease progression by promoting regeneration, releasing growth factors and clearing myelin debris in a process called phagocytosis, which is key for remyelination.
Animal models of MS include the well-characterized dietary administration of cuprizone, a copper-binding toxin, which enables the study of molecular mechanisms of demyelination/remyelination. Cuprizone causes death of oligodendrocytes and demyelination in brain areas such as the corpus callosum, which links the two sides of the brain. Replacement of cuprizone by normal food is followed by remyelination.
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.
mCSF promotes survival, proliferation and differentiation of cells involved in myelin damage and repair, while it also shifts microglia toward an anti-inflammatory profile favoring remyelination.
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