King's College London scientists say that blocking the release of chemical glutamate in the brain may help prevent Parkinson's disease.
Dr. Susan Duty said that 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 this chemical changes the way these pathways operate, and makes movement even less well controlled.
She said that stimulating 'trigger points' responsible for the release of a chemical that can kill brain cells can help thwart Alzheimer's.
"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," said Duty.
"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.
"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," she added.
Duty said that current drugs could only 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," she said.
"However, they do little to combat the ongoing progressive cell death meaning that symptoms get worse, higher doses of drug are needed to control the worsening symptoms, the result being appearance of disabling side-effects such as involuntary flailing limb movements and painful twisting of joints.
"Given the disease is progressive in nature, the continued death of cells in the substantia nigra leads to gradual worsening of symptoms and decline in patients' quality of life over time.
"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," she added.
The study was presented at The British Pharmacological Society's Summer Meeting in Edinburgh.