A “HOLY Grail” molecular target has been discovered to protect nerves from damage in multiple sclerosis (MS), a Scottish university study has said.
The research also said a common diabetes drug could help enhance this new-found natural mechanism and prevent disability progression.
Scotland has one of the highest MS rates in the world. In people who have the neurological condition, the protective coating surrounding nerves known as myelin is damaged, causing them to become less energy efficient.
This makes the nerves vulnerable to further damage and causes disability over time, the MS Society said.
The University of Edinburgh carried out a research programme spanning more than a decade, partly funded by the society. It discovered a natural mechanism in the body that tackles the myelin issue, which they are calling ARMD (axonal response of mitochondria to demyelination).
Researchers said this natural function alone does not provide enough energy to address demyelination, but its discovery raised the possibility of using a drug to enhance it. After further research, the team was able to enhance ARMD and protect the vulnerable nerves using the diabetes drug pioglitazone.
Lead author, Dr Don Mahad, a senior clinical lecturer at the university, said: “Although our understanding of MS has vastly improved over the last two decades, new therapies still do not protect nerve fibres.
“Such protection is the Holy Grail in MS treatment – not only for the relapsing form of MS, which has various options available, but for progressive forms too, where treatment continues to lag behind.
“Remarkably, we were able to enhance ARMD and protect these vulnerable nerves using the readily available diabetes drug pioglitazone.
“This is an incredibly important discovery – one we believe could finally bridge the gap in MS treatment.”
MS Society assistant director of research Dr Emma Gray said the find could mean no-one will need to worry about their MS getting worse, adding: “This is another important stride towards our goal of stopping MS.”
The research is published in the journal Acta Neuropathologica.
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