April 20, 2023
Fractalkine: A Potential MS Therapeutic that Enhances Repair and Regeneration
- Funded by MS Canada
Summary: Researchers found that an immune system molecule called fractalkine promoted repair of myelin, the protective coating surrounding nerve fibers, in the brain of mice with multiple sclerosis-like disease. The findings of this study demonstrate fractalkine as a potential therapeutic for multiple sclerosis to enhance repair and regeneration.
Background: Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) that involves damage or loss of myelin, the protective coating of nerve fibers in the brain and spinal cord. There is a need for effective MS therapeutics that regenerate the brain and spinal cord and promote the production of myelin (or remyelination). In animal models, fractalkine was previously shown to be a critical regulator of oligodendrocytes, cells that produce myelin and enhance regeneration and remyelination in the CNS (read more – here). Fractalkine represents a potential therapeutic pathway for remyelination to further investigate in MS.
Details: In a recent study funded by MS Canada, Dr. Anastassia Voronova (University of Alberta) and team aimed to examine whether fractalkine would enhance brain regeneration and remyelination after a demyelinating injury, resulting in damage or loss of myelin. The researchers used healthy mice that were provided with a cuprizone diet to induce MS-like disease and demyelination (injury) and were then given fractalkine infusions as treatment to determine its effect.
Results: The researchers found an increase in the production of oligodendrocytes and the cells that generate oligodendrocytes called oligodendrocyte precursor cells (or OPCs) following fractalkine treatment. Importantly, this led to remyelination in the brain of fractalkine-treated mice. There was also a reduction in microglia cells that cause inflammation in the brain.
Impact: This study identifies a novel molecule, fractalkine, that promotes remyelination in a MS mouse model. Learnings from this study will be important for the development of effective remyelinating therapeutics and strategies for MS.