Important findings linking the protein Connexin 36 with the disrupted communication between nerve cells in Parkinson’s patients may contribute to a better understanding of the disease.
The study was developed by Bettina Schwab, a former Ph.D. student at The Netherlands’ University of Twente Faculty of Electrical Engineering, Mathematics, and Computer Science (EWI), who defended her dissertation on April 22 as part of the Parkinson’s disease, computational neuroscience, and synchrony symposium.
The human brain is composed of millions of nerve cells, called neurons, that form the white and grey tissue masses. The communication of the brain cells with each other and with the remaining parts of the body is accomplished through the release of molecules called neurotransmitters.
Disruption in the transmission of these signals often leads to the synchronization of nerve cells, in which all neurons start doing the same thing — impairing the stimuli produced by the brain to reach the remaining parts of the body.
Although the cause of Parkinson’s disease (PD) is not fully understood, it is established that the lack of dopamine in the basal ganglia of Parkinson’s patients, a region in the base of the brain that controls a variety of functions including voluntary motor movements, leads to PD symptoms that include muscle rigidity, slowness of movement, balance problems and tremors.
Although medication that balances the lack of dopamine is given to PD patients, it has several side effects and isn’t always effective, revealing the need for new therapeutic approaches.
The research carried out during Bettina’s Ph.D. work revealed a new molecule that may be linked to the perturbations found in Parkinson’s patients. After analyzing brain samples from 12 deceased individuals, half of whom had PD, she found that Parkinson’s patients had higher levels of Connexin 36, a protein that is involved in the connection of neurons through gap junctions or synapses.
The investigators from The Netherlands believe that the connection established by this protein may play a part in the synchronization of nerve cells that occurs upon the development of dopamine deficiency.
Such findings may be a crucial contribution to better understand how Parkinson’s disease develops and to create more efficacious therapies that control the motor problems found in Parkinson’s patients.