Parkinson's hope in hypertension drug

A drug used to treat hypertension could prevent progression of Parkinson's disease, suggest findings of a mouse study.

Blocking calcium channels with the drug isradipine (Prescal) could rejuvenate dopamine receptors, potentially slowing progression of early-stage Parkinson's disease, it found.

Dopamine-containing neurons inside the substantia nigra region of the brain are destroyed in Parkinson's patients, but the reason for this has been unknown.

But this US research suggests that the neurons rely on calcium channels to maintain their rhythmic activity. High levels of calcium in the channels of dopamine neurons could cause the neuronal damage seen in Parkinson's disease.

For the study, juvenile mice genetically engineered to develop Parkinson's were studied to see if dopaminergic neurons could be rejuvenated. The mice had a biodegradable pellet containing the calcium antagonist isradipine or placebo implanted under their skin for a week.

The mice were culled and brain slices taken. This revealed that dopamine neurons were protected from lethal toxins by isradipine but the naive neurons were not.

Another commonly used experimental model of Parkinson's in mice, based on injection of the toxin 1-methyl-4-phenyl-tetrahydropyridine (MPTP), was then performed. MPTP works by crossing the blood- brain barrier before being taken up by the dopaminergic neurons, which it then destroys.

Healthy mice treated with isradipine or placebo were given repeated injections of MPTP over a period of five weeks.

Isradipine treatment was found to almost halve the number of dopaminergic neurons that were lost as a result of the toxin effects of MPTP, compared with the control mice.

They concluded that blocking calcium channels in adult neurons induced a more juvenile form of neural activity, forcing the neurons to use other ion channels and thereby protecting against the progression of Parkinson's.

Lead researcher Professor James Surmeier, from the department of physiology at Northwestern University in Chicago, said: 'These findings point to a potential therapeutic strategy that might protect against Parkinson's disease in humans, and possibly also broaden the therapeutic window for patients in the early stages of the disease.'

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