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New study provides deeper insight on Parkinson's disease

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ANI Washington

Scientists have gained new information on what causes the Parkinson's disease.

Dopamine is an important neurotransmitter which affects physical and psychological functions such as motor control, learning and memory. Levels of this substance are regulated by special dopamine cells. When the level of dopamine drops, nerve cells that constitute part of the brain's 'stop signal' are activated.

Jakob Kisbye Dreyer from University of Copenhagen explained that presence of dopamine was crucial in the system to block the stop signal. Parkinson's disease arises because for some reason the dopamine cells in the brain are lost, and it is known that the stop signal is being over-activated somehow or other. However, they could now use advanced computer simulations to challenge the existing paradigm and put forward a different theory about what actually took place in the brain when the dopamine cells gradually died.

 

Scanning the brain of a patient suffering from the disease revealed that in spite of dopamine cell death, there were no signs of a lack of dopamine, even at a comparatively late stage in the process.

The researchers said that as per their calculations, cell death only affected the level of dopamine very late in the process, but that symptoms could arise long before the level of the neurotransmitter started to decline. The reason for this was that the fluctuations that normally made up a signal became weaker. In the computer model, the brain compensated for the shortage of signals by creating additional dopamine receptors. This had a positive effect initially, but as cell death progressed further, the correct signal might almost disappear. At this stage, the compensation becomes so overwhelming that even small variations in the level of dopamine trigger the stop signal, which could therefore cause the patient to develop the disease.

The findings have been published in the Journal of Neuroscience.

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First Published: Sep 17 2014 | 4:53 PM IST

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