Canada Kicks Ass - Enzyme find could fight MS

McGill doctoral student Athena Kalyvas, working on laboratory mice, found that controlling an enzyme in the animals also turns off symptoms and progression of MS.

Montreal researchers have identified a key factor in multiple sclerosis, a devastating disease of the nervous system.

News that controlling an enzyme could "turn off" the autoimmune disease represents fresh hope for the 35,000 Canadians who suffer from MS's debilitating symptoms.

The enzyme has been shown to control the onset and progression of MS in mice, Sam David, a McGill University Health Centre neuroscientist, said.

"Blocking this enzyme has a remarkable effect in preventing disease and relapses," said David, a McGill University medical professor whose findings are to be published today in Neuron, a neuroscience journal.

"That means this particular enzyme is certainly a very good target for drugs" that would block MS, he added.

In MS, the body's immune system attacks the myelin, the insulating membrane surrounding nerve fibres. Scarring - or sclerosis - impedes muscle co-ordination and vision, and can lead to paralysis.

The causes of MS is unknown.

David's discovery stems from eight years of research in an area unrelated to MS - the role of iron in molecules after injury.

"We began to look at this particular enzyme (cPLA2) and whether it calls in the immune cells to help clean up the debris, which is what you want after injury," he said.

In MS, there's an abnormal influx of these immune cells.

Not only was the enzyme present in mice with MS lesions, but treatment with a chemical inhibitor of the enzyme halted the disease.

"It's a most exciting feeling - a eureka moment," David recalled of watching a hypothesis bear fruit in laboratory experiments done by his doctoral student, Athena Kalyvas.

But it's only a first step, he cautioned: "There's no way to predict whether it will work in humans."

Current therapies focus on ways of reducing the frequency of MS attacks and on slowing the progression of disability, said Deanna Groetzinger of the Multiple Sclerosis Society of Canada, which funds such research projects.

Other studies are looking at ways to stimulate nerve cells to produce new myelin.

Current therapies are most effective early on in the disease, before severe disability sets in.

"But it's never 100 per cent. There's no guarantee you won't get worse over time," Groetzinger said. "MS is a complex disease, so this is really a promising step forward.

"If this discovery could prevent the disease, that would be a good-news story."

The next step is to move from mice to humans to ensure the treatment is safe and effective.

cfidelman@thegazette.canwest.com