The following correction was printed in the Guardian's Corrections and clarifications column, Wednesday October 10 2007

The article below said that Huntington's disease is triggered by the misfolding of the Huntington protein, which clumps together if both copies of the gene which codes for it are defective. This implied that it is a recessive disease and that both copies of the gene need to be defective to cause it, but Huntington's is an autosomal dominant disease, which means that only one gene copy needs to be defective for the disease to manifest itself.

Scientists have made a breakthrough in the search for a cure for Huntington's disease. Hope for a future treatment has been raised by the discovery of a chemical that slows damage to the brain caused by the genetic disease.

The researchers do not yet know how the chemical works, because it was originally discovered during a trial and error trawl through tens of thousands of compounds, but they hope that by working out what it does it will open up a whole new avenue of potential treatments. So far the researchers have shown that the chemical improves symptoms in mice that have a form of the disease.

Huntington's disease is an inherited condition which affects a patient's movement, perception and behaviour. Most patients have around 40 years of unaffected life before developing symptoms, but there is currently no cure. Between 6,500 and 8,000 people in the UK have the disease, according to the NHS.

The symptoms are caused by the buildup of protein in the brain. These are triggered by the misfolding of the huntingtin protein, which clumps together if both copies of the gene which codes for it are defective. To look for chemicals that might prevent the formation of these protein clusters researchers in the US tested tens of thousands of random compounds in yeast cells that carried the mutant gene. This "high throughput screening" was designed to identify those chemicals that prevented the build up which causes the damage.

The tests yielded a couple of promising chemicals, one of which, C2-8, has now been use in experiments on mice that exhibit the symptoms seen in humans. "To go from yeast to animals is a pretty big step," said Steven Hersch at Harvard Medical School, "The results were certainly beneficial in that they slowed down the development of symptoms in the mice and they improve the neuropathologic findings in the mice."

Disappointingly, although C2-8 does seem to hold the symptoms it did not actually prolong the lives of the mice. But Prof Hersch said it was early days yet. A chemically similar molecule might be more effective and by understanding how it worked researchers hoped to open up new angles for potential new treatments. "We can find what this compound does and from that knowledge find other approaches for therapy," said Prof Hersch.

The results are published today in the Proceedings of the National Academy of Sciences.

Backstory

The NHS estimates there are 6,500 to 8,000 sufferers in the UK. The disease was first described by the US doctor George Huntington in 1872, and originally named Huntington's chorea after the Greek word for dancing because of the jerky, involuntary movements it causes. Symptoms typically first appear between 30 and 50 years of age. They include mood swings and bizarre behaviour often not attributed to the disease, which typically kills within 10 to 20 years.