Molecule triggers remyelination in MS in new study

A signalling protein called fractalkine promoted myeline repair in a new study in a mouse model of multiple sclerosis (MS).

Fractalkine triggered new growth of myelin-producing cells, oligodendrocytes, and also reduced pro-inflammatory immune cells in the brain.

The protein has been shown in previous studies to help stimulate oligodendrocyte precursor cells to turn into mature oligodendrocytes more quickly. This was supported by other animal studies that showed fractalkine could help protect nerve fibres before MS began.

For the study, mice were fed cuprizone for six weeks, which causes loss of myelin. Fractalkine was then infused directly into their brains for three days. The mice were then given a normal diet to allow myelin formation to begin.

Oligodendrocyte precursor cells and mature oligodendrocytes increased up to double the amount in the treated mice. The molecule also reduced the number if immune cells that travels round the brain and spinal cord and is thought to contribute to MS – pro-inflammatory microglia. Fractalkine also increased myelin density.

Testing found that fractalkine acts on the microglia and the oligodendrocyte precursor cells to increase oligodendrocyte formation. It also caused microglia to clear myelin debris in order to clear the way for new myelin.

The study’s authors said that fractalkine now ‘represents a novel candidate for remyelination strategies.’ It will be tested in mouse models of other diseases that are neurodegenerative, and research will aim to uncover a suitable way to deliver the molecule to the brain.