An international team of scientists based at Queen’s University Belfast has discovered a potential way to repair the nerve damage responsible for multiple sclerosis.
Researchers say the “landmark discovery” could lead to the first treatments that reverse the course of MS and other debilitating neurological disorders.
“Current therapies can limit or stop relapses in MS patients but they cannot repair the damage,” said Yvonne Dombrowski of Queen’s. “Our approach could repair damage as well as reducing attacks.”
The study, published in Nature Neuroscience, shows how immune cells called regulatory T-cells, or “T-regs”, can release a protein known as CCN3, which stimulates the rebuilding of myelin, a protective sheath that surrounds nerve fibres.
Autoimmune attacks can destroy myelin, causing symptoms of MS such as vision loss, pain and paralysis.
Although the research took place with laboratory mice and a human version of the procedure has not yet been developed for clinical trials, the Queen’s researchers said a treatment based on T-regs and CCN3 could “revolutionise” MS therapy.
MS is the most common neurological disease among young adults, affecting an estimated 2.3m people worldwide. A dozen drugs, with total annual sales of around $20bn, are available today to alleviate symptoms of MS, slow down its progression or reduce the severity and severity of relapses.
Companies producing MS treatments include Biogen, Novartis, Teva and Sanofi. “This exciting study gives us an important understanding of how myelin repair can be promoted, which could open up new areas for treatment development,” said Sorrel Bickley, head of biomedical research at the MS Society, the UK charity focusing on research and support for people affected by the disease. “We welcome this international collaboration led by Northern Ireland, where rates of MS are among the highest in the world,” she added. More than 4,500 people in Northern Ireland are affected by MS.
The Queen’s scientists, working with researchers at universities in England, Scotland, Ireland, France and the US, carried out a series of experiments with mice genetically engineered or chemically treated to develop the rodent equivalent of MS.
They first discovered that when T-reg immune cells are transplanted into MS mice, missing myelin begins to grow back. This recovery takes place because T-regs stimulate stem cells in the brain to mature into oligodendrocytes, the specialist cells that make myelin.
On further investigation, the researchers found that T-regs achieved this effect by secreting CCN3 — and that treatment with the protein on its own led to regrowth of myelin in mice. CCN3 was previously known as one of many molecules involved in regulating cell growth, but not recognised as a promoter of myelination. Further studies with human T-reg cells will be required to pave the way for clinical trials of CCN3 or a drug derived from it, said Dr Dombrowski. “We don’t want to raise hopes prematurely in MS patients,” she added.