Current treatment of multiple sclerosis is based on modulating the activity of the immune system, or preventing its cells from accessing the central nervous system and damaging it. These therapies are effective in the early phases of the disease, but they do not prevent its advance and the progressive functional deterioration. However, a new discovery could change that by reducing damage caused by MS.

During the progressive phase of the disease it is the microglial cells in the brain that are the main cause of the chronic inflammation responsible for the neurological deterioration. These microglial cells are the brain's sentries and react when faced with any damage or infection in the brain. This reaction, which is in principle beneficial, becomes harmful when it is prolonged over time, leading to chronic inflammation, and aggravates the disease and encourages its progression.

A study by an international research group coordinated from the Basque Autonomous Community identified a receptor known as P2X4 present in the microglial cells that increases their anti-inflammatory potential in order to reduce the damage in MS and encourage the body's own repair responses.

The blocking of P2X4R signals worsened clinical signs in mouse model MS, favored microglia activation of inflammation, and inhibited myelin debris elimination. Moreover, P2X4R blocking in microglia halted oligodendrocyte differentiation in vitro and remyelination after lysolecithin‐induced demyelination. Conversely, activation of P2X4R signals by ivermectin (IVM) favored a switch in microglia to an anti‐inflammatory response, activated myelin debris elimination, promoted the remyelination response, and reduced clinical signs of mouse model MS. The results provided evidence that P2X4Rs modulate inflammatory responses, and identify IVM as a potential candidate among currently used drugs to promote the repair of myelin damage.

Results of mouse model studies sometimes do not translate to humans and may be years away from being a marketable treatment. However, the researchers said it was possible that the drugs that activate this receptor may improve the symptoms during the chronic phase of the disease when furthering the repair of the nervous tissue.

The findings were published in the journal EMBO Molecular Medicine.