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Drugs commonly used to treat high blood pressure may slow or even halt the progression of Parkinson’s disease, scientists said today.
If the results from animal studies are confirmed in humans it could be the biggest advance in managing the disease for 30 years.
Although treatments are available to reduce the symptoms of Parkinson’s, they become less effective over time and nothing currently can stop the disease progressing.
The new research holds out the prospect not only of slowing Parkinson’s but preventing the symptoms ever appearing, according to the American team.
Parkinson’s, which mainly affects people aged 60 and over, occurs when dopamine neurons in the brain start to die. Dopamine released by the cells is a critical chemical messenger that affects the control of movement. When dopamine is lacking, movement becomes more difficult and uncoordinated. Sufferers experience muscle rigidity and tremors and ultimately lose the ability to walk, talk or even pick up a glass of water.
An estimated 10,000 people in the UK are newly diagnosed each year with Parkinson’s and up to 120,000 have the disease.
Scientists at Northwestern University in Chicago discovered that isradipine, a “calcium blocker” drug for high blood pressure, angina and stroke, had the power to rejuvenate ageing dopamine neurons. Tests on mice showed that the drug protected the dopamine cells from toxins that would normally kill them. The cells began to operate as if they were younger. As a result, mice engineered to have a progressive Parkinson’s-like disease resisted becoming ill.
Professor James Surmeier, the leader of the study whose findings are published today in the online version of the journal Nature, said: “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. It would be like taking a baby aspirin everyday to protect your heart.”
Using the drug, or other calcium blockers like it, could also extend the effectiveness of traditional dopamine-boosting medication - possibly doubling or tripling the length of time in which it worked, said Professor Surmeier, who has been researching Parkinson’s disease for 20 years. This in itself would be a “huge advance”, he said.
The team’s key discovery was that young and old dopamine neurons operate in entirely different ways. While the young cells use sodium ions - charged atoms - to generate electrical signals, with advancing age they switch to calcium ions. Calcium ions are “wild” and have to be kept under control, said Professor Surmeier. “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,” he explained. When isradipine was used to block the “gateways” through which calcium ions entered the cells, the neurons reverted to their youthful behaviour. After a short ’silent’ interval they went back to using sodium and became calmer.
The scientists are now planning to launch a clinical patient trial.
Dr Kieran Breen, director of research and development at the Parkinson’s Disease Society, welcomed the findings but cautioned that much more work still had to be done.
“This study appears to suggest that calcium plays a role in the death of nerve cells, as isradipine blocks calcium’s route into the cells in the brain and changes how they behave. Too much calcium within the cell makes them more fragile and more likely to be sensitive to the effects of toxic external factors.
"However, the results that have been reported are from a very early stage pre-clinical trial using a model of Parkinson’s. Further trials are needed to establish whether similar results are seen in people with the condition.
“It is too early to state with confidence that this drug will be appropriate for the treatment for Parkinson’s disease. We can also not predict whether this drug will be used as a preventative or protective measure in the future. A significant amount of further research will be required before any definite conclusions can be drawn.”
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