Disrupted ‘Stress-Coping’ Mechanism in the Brain Linked to Parkinson’s Disease

A malfunctioning mechanism to cope with intense brain activity plays an important role in the development of Parkinson’s disease. That is the conclusion of a study by Professor Patrik Verstreken (VIB / KU Leuven) and his team.

Parkinson's Disease
A disrupted 'stress-coping' mechanism in the brain can cause damage to the synapses that transmit electrical brain signals.

The synapses in our brains are constantly transmitting enormous amounts of electrical signals – up to 800 in just one second. To process all these signals, our brain uses various mechanisms to cope with the stress of intense brain activity. Professor Verstreken’s team has now discovered that one of these coping mechanisms does not function properly in Parkinson’s disease.

“The genetic mutations that cause Parkinson’s disease affect the stress-coping mechanism of the synapses,” says Professor Verstreken. “As a result, the synapses sustain damage, which in turn disrupts the transmission of brain signals and ultimately leads to neurodegeneration. Our study is the first to specifically link dysfunctional synapses to Parkinson’s disease.”

Building on the results of this study, the scientists want to find out how universal this disruption of the stress-coping mechanism is. “To understand the mechanism of Parkinson’s disease, we’ve mostly been using fruit flies. Our colleagues at the European Neuroscience Institute in Göttingen, led by Ira Milosevic, have already made similar discoveries in the neurons of mice. Now we can examine whether the same stress-coping mechanism is disrupted in the brain of human patients as well. In any case, our study shows that maintaining synaptic function will be crucial in the fight against Parkinson’s disease.”

“Next, we hope to find ways to restore normal synaptic communication. By reactivating the stress-coping mechanism, we might also be able to repair the damage to the synapses. But this, of course, will require further research.”

Click here to read the study in Neuron