New research could lead to drugs that repair the damage caused by multiple sclerosis (MS).
Scientists have identified a biochemical "switch" that helps stem cells in the brain fix injured nerves. In future, medicines targeting the same pathway might provide a way to halt or even reverse the disease.
The discovery was described on Sunday as "one of the most exciting developments in recent years" by the head of an MS charity.
It points the way to radical new regenerative treatments for the auto-immune disease which affects almost 100,000 people in the UK.
Multiple sclerosis occurs when the body's own immune system attacks and destroys the fatty insulating material, called myelin, that coats nerve fibres. Nerve messages are jumbled or interrupted leading to symptoms ranging from mild numbness to crippling paralysis.
In people with MS, the natural process by which lost myelin is rebuilt and replaced is blocked. Scientists have been looking for ways to switch the mechanism back on by focusing on oligodendrocyte precursor cells (OPCs), a type of stem cell needed for myelin repair.
A major problem is that OPCs can migrate to the area of injury but fail to develop into the oligodendrocyte cells that restore myelin. The new research has identified a biochemical signalling pathway which triggers OPC transformation.
Tests on rats showed that blocking a cell molecule called retinoid acid receptor RXR-gamma prevented the differentiation of OPCs into oligodendrocytes. Conversely, stimulating RXR-gamma with a special form of retinoic acid switched on the transformation of OPCs and ultimately led to the repair of damaged nerves.
The research, part-funded by the MS Society, is published in the journal Nature Neuroscience.
Professor Robin Franklin, director of the MS Society's Cambridge Centre for Myelin Repair at Cambridge University, who led the study, said: "Therapies that repair damage are the missing link in treating multiple sclerosis. In this study we have identified a means by which the brain's own stem cells can be encouraged to undertake this repair, opening up the possibility of a new regenerative medicine for this devastating disease."