New research in mice suggests that poor recycling of cholesterol in the brain impairs the repair of myelin, the protective coat surrounding nerve cells that is lost in multiple sclerosis (MS).
Pharmacological stimulation of cholesterol synthesis by brain immune cells — called microglia — boosted the regeneration of myelin, supporting its potential as a new therapeutic strategy for MS.
The study, “Microglia facilitate repair of demyelinated lesions via post-squalene sterol synthesis,” was published in the journal Nature Neuroscience.
MS is characterized by the loss of myelin, a cholesterol-rich sheath that protects nerve cells. Damaged or defective myelin in the central nervous system or CNS, comprised of the brain and spinal cord, release cholesterol-rich myelin debris that is taken up and recycled by microglia. These immune cells of the brain use that debris for the production of new myelin, which is mediated by myelin-producing cells called oligodendrocytes.
“This efficient repair mechanism probably takes place all the time in healthy individuals,” Gesine Saher, at the Max Planck Institute for Experimental Medicine in Göttingen, Germany, and the study’s lead author, said in an institute press release.
Here, the researchers investigated whether the production of sterols, like cholesterol, in different cell types of the CNS play a role in the repair of demyelinated lesions.
The team analyzed the corpus callosum, the area that connects the two sides of the brain, in cuprizone-treated mice (an animal model of MS) at two stages of demyelination — both acute and chronic — and remyelination.
The analysis of cholesterol-related genes revealed that cholesterol synthesis in microglia cells was required for remyelination after acute, or early, demyelination.
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