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Hitting cell hot spot to stop excess glutamate could help thwart Parkinson's disease

Parkinson's disease is a degenerative brain disorder that is triggered by death or degeneration of nerve cells in a part of the brain called substantia nigra. This brain region is essential in maintaining normal movement, so when the cells start to die off, patients lose the ability to properly execute and control movements.

Dr Susan Duty from King’s College London is aiming to find a way to slow down, stop or – even better – reverse the cell death process. Her latest work, aimed at stimulating ‘trigger points’ to stop the release of a chemical that can kill brain cells, was presented recently at The British Pharmacological Society’s Summer Meeting in Edinburgh.

Dr Duty says one of the contributing factors to nerve cell death is an excess of the chemical glutamate in the motor control pathways in the brain. An excess of glutamate changes the way these pathways operate and makes movement less well controlled but, more importantly, glutamate is one of the factors considered responsible for the demise of the brain cells. At the meeting, Dr Duty presented her latest work on ways to stop glutamate being released.

Dr Duty said: 'The way we hope to achieve this is by stimulating protein targets on the nerve cell called metabotropic glutamate receptors. Certain types of these receptors, when stimulated, are known to prevent release of glutamate in other brain regions. We, and others, have now taken these ideas into regions relevant to Parkinson's disease in the hope of reversing both the clinical signs and cell death associated with this condition.'

According to Dr Duty, current drugs can treat the symptoms but not the underlying cause of the disease: 'They provide relief of symptoms by replacing the chemical, dopamine, which the dying cells would normally secrete in order to maintain proper control of movement.

'However, they do little to combat the ongoing progressive cell death meaning that symptoms get worse… Finding drugs that can provide protection or repair to the dying cells – as well as relieve the clinical signs of Parkinson's – is therefore a key area of interest in this field.'

Dr Duty and colleagues have recently published findings showing that stimulating certain classes of metabotropic glutamate receptor can reverse symptoms in a preclinical model of Parkinson's disease.

'More recently, we have identified which specific type of receptor is involved,' she says. 'By targeting specific receptors it is hoped that side-effects will be minimised as fewer targets elsewhere in the brain will be stimulated.

'We also have good evidence now that stimulating these receptors can provide protection to the dopamine-containing nerve cells in preclinical models of Parkinson's disease and that the protected nerve cells function normally and are able to help restore movement control.'

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Pharmacology/ Therapeutics


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