Cell batteries offer clues to MS
Scientists have discovered a way that the body can protect itself from damage linked to multiple sclerosis (MS), accelerating the search for treatments.
The research shows that cells recruit mitochondria – the cell’s main source of energy – to damaged areas to aid repair.
Findings in animal studies further suggest that a common diabetes drug could help boost this natural mechanism and prevent the disease worsening.
Researchers say their results are key step in the search for a drug target to help treat MS patients.
The study focused on the protective coating that surrounds nerves in the brain and spinal cord, known as myelin. MS causes loss of myelin, making nerves less efficient and vulnerable to further damage.
Preventing loss of myelin – known as demyelination – and repairing its effects is a key goal in the search for a treatment for MS.
More than 130,000 people in the UK live with MS, a debilitating condition that can cause difficulties with everyday tasks such as dressing, walking and speech.
Researchers at the Centre for Clinical Brain Sciences say the mechanism – which they have named axonal response of mitochondria to demyelination (ARMD) – means that more energy is available to the cell where it is most needed.
The scientists found that although the mitochondrial response is not enough to repair damage in MS, mimicking or boosting its effects could be key to treating demyelination.
In a follow-up study they showed that a drug currently used to treat Type II diabetes boosted the mechanism in mice.
Using drugs that are already approved for other conditions is encouraging as it can mean that clinical trials are carried out more quickly.
The researchers caution that more work is needed before the drug could be used in patients but say that it paves the way for further studies into treating MS.
The study was funded by the MS Society and is published in the journal Acta Neuropathologica.
Disability in MS is caused by a loss of nerve fibres following damage to the myelin that protects them. Although our understanding of MS has vastly improved over the last two decades, new therapies still do not protect nerve fibres. Remarkably, we were able to enhance ARMD and protect these vulnerable nerves using the readily available diabetes drug. This is an incredibly important discovery – one we believe could finally bridge the gap in MS treatment.
This represents another important stride towards our goal of stopping MS – and we believe that MS treatment could in the near future look completely different. Currently, there are no effective neuroprotective therapies available for MS, but Dr Mahad’s research demonstrates we are getting closer – and finding treatments for everyone with MS is now a very real prospect.