The finding could enable doctors to add isradipine to their arsenal of weapons against Parkinson's disease, where the death of dopamine-releasing nerve cells causes debilitating movement difficulties in sufferers.

Prof. James Surmeier and his team of scientists at Northwestern University, US, examined the effects of isradipine, a calcium channel blocker of the dihydropyridine class, on neurons.

They discovered that the drug restores stressed-out dopamine neurons to their vigorous younger selves, and could slow or even halt the progression of Parkinson's. Dopamine is a neurotransmitter that is critical to a person's ability to direct their movements. As neurons die and dopamine levels drop, movement becomes increasingly difficult, eventually consigning the patient to a wheelchair, unable to talk. Parkinson's is the second most common neurodegenerative disorder in the US, affecting around one million people.

"There has not been a major advance in the pharmacological management of Parkinson's disease for 30 years. Our hope is that this drug will protect dopamine neurons, so that if you began taking it early enough, you won't get Parkinson's disease, even if you were at risk," said Prof. Surmeier, who heads a Parkinson's disease research centre at Northwestern.

"It would be like taking a baby aspirin everyday to protect your heart."

Isradipine could also help those who already have the disease. In animal tests, Prof. Surmeier found that the drug protects dopamine receptors from toxins by restoring them to a state where they are less vulnerable.

Currently, Parkinson's patients take L-DOPA, which is converted in the brain to dopamine. However, the therapy becomes less effective over time and the increasing doses leads to side-effects including involuntary movements.

Prof. Surmeier hopes isradipine could double or triple the therapeutic window for L-DOPA, which he described as a "huge advance". He has been researching Parkinson's for two decades and in that time, he became increasingly frustrated at the lack of progress regarding how or why dopamine neurons die in the disease.

He decided to investigate whether the electrical activity of the neurons might provide a clue. It was already known that the cells are pacemakers - they work constantly, generating regular electric signals. However, when he looked deeper he discovered a curious phenomenon.

Most pacemaker cells use sodium channels to work, but dopamine neurons use calcium channels.

"The reliance upon calcium was a red flag to us," Prof. Surmeier said. The calcium ions need to be chaperoned by the cell to prevent them "causing trouble", as he put it. The cell has to sequester them or keep pumping them out, which takes a lot of energy.

"It's a little like having a room full of two year olds you have to watch like a hawk so they don't get into trouble," Prof. Surmeier said. "That's really going to stress you."

He thought that non-stop stress on the neurons might explain by they become vulnerable to toxins and die more rapidly as we age. But, like so often ion science, it was a serendipitous discovery that led him to a possible therapy.

While working on a different problem, Prof. Surmeier discovered neurons do, in fact, use sodium - but only when they young. As the cells age, they stop producing sodium and become increasingly reliant on calcium to function.

By using a drug that blocks calcium's route into cells, Prof. Surmeier discovered a way to force the neurons to start using sodium again.

When he gave the mice isradipine, the dopamine neurons at first became silent. Then, within a few hours, they began using sodium again.

"This lowers the cells' stress level and makes them much more resistant to any other insult that's going to come along down the road. They start acting like they're youngsters again," concluded Prof. Surmeier.

Next, the scientists hope to test their theory in human clinical studies.

"This animal study [now published in Nature] suggests that calcium channel blockers, drugs currently used to reduce blood pressure, might someday be used to slow the steady progression of Parkinson's disease," said Dr Walter Koroshetz, deputy director of the National Institute of Neurological Disorders and Stroke (NINDS).