MS drug shown to promote remyelination in mouse study
Spasticity medication Baclofen promoted the repair of myelin in a mouse model of multiple sclerosis (MS), a new study has found.
Most treatments for MS focus on controlling the immune system to help prevent relapses, but repairing myelin – the protective sheath around the nerves which is damaged by MS – is for some researchers the holy grail.
In another study, baclofen was found to stimulate oligodendrocyte precursor cells (OPC) to mature via activation of GABA type B receptors. GABA is a chemical messenger in the brain and spinal cord and is a key regulator of OPC maturation and myelin production.
In this study, one disease model saw lab-grown mouse and rat brain slices exposed to lysolecithin (LPC), a molecule that causes demyelination. Another saw mice have LPC injected into their spinal cord to mimic MS.
Treatment with baclofen for six days while LPC exposure was happening increased myelin-associated glycoprotein and myelin basic protein, both of which rose to almost healthy brain levels.
This was not due to changes in the number of OPCs or matured oligodendrocytes, said the researchers, which indicated GABA activation “promotes myelin generation by mature [oligodendrocytes] without affecting OPC [growth] capacity.”
The researchers then looked at the results of seven days of baclofen treatment in mice when lysolecithin had been given five days before. The medication caused a significant increase in OPC maturation and the amount of remyelinated nerve fibres.
The team said these results show that baclofen may be a potential therapy for stimulating myelin repair in MS. Although it is an important first step, more research is needed, they said.