To understand Parkinson’s Disease, it is important to understand the brain and its function related to the disease. Parkinson’s Disease is a progressive disease of the Central Nervous System, progressive meaning that symptoms, such as slowness of movement (bradykinesia), stiffness and tremors, and more will progress and worsen overtime. When dopamine producing neurons in a part of the brain called the substantia nigra begin to die, these symptoms will start to occur. Dopamine is a neurotransmitter, meaning that it is a chemical that conveys information between neurons by attaching to specific sites either within the brain or other parts of the nervous system. Dopamine plays a key role in controlling movements. Neurons are cells of the nervous system that are responsible for sending and receiving messages between the brain and the rest of the body. They are much like the electrical wiring in your home that signals the light to turn on when the switch is flicked. When 80 percent of these dopamine producing neurons are lost, Parkinson’s Disease will develop.

Annelies J.M. van Nuland and his colleagues (2019) suggested that GABA may play a regulatory role in the physiological processes associated with Parkinson’s disease.  GABA, short for gamma-aminobutyric acid, is a major inhibitory neurotransmitter meaning that it blocks certain communication between nerve cells in the brain. The researchers of this study predicted that there would be less GABA, in a region of the brain known as the thalamus, in Parkinson’s patients who experience tremors compared to those patients who do not. A tremor is an uncontrollable movement or shake that mostly occur at rest. The thalamus acts as a relay station for information going to and from different regions of the brain. This prediction was based on previous research findings.

To collect evidence to test this prediction, the researchers tested four groups of individuals: 60 Parkinson’s disease patients in total, with dopamine resistant tremors, with dopamine responsive tremors, non-tremor patients and lastly a group of healthy patients. All individuals were given two separate treatments: on one day, they received a drug (levodopa-benserazide) and on the second day they received a placebo, a substance that resembles the drug but will have no effect on the person taking it. All individuals involved in the study were examined for three main symptoms of Parkinson’s disease: bradykinesia (slowed movement), rigidity (stiffness) and tremors. Along with looking at these symptoms, each person had a picture of their brain taken using MRI technology to determine the involvement of the thalamus, motor cortex and visual cortex or non-motor region in the brain. All measurements were taken on both on and off days (when participants had taken/not taken the drug).

Although the researchers expected Parkinson’s patients to have higher GABA levels in the thalamus than healthy participants, the results of this study did not match their prediction. There was no major difference in the levels of GABA in the 60 participants with Parkinson’s disease compared to the 22 healthy patients. The evidence collected from the study suggests that there is a relationship between the GABA concentrations in the motor cortex area of the brain and how severe the disease is. In fact, lower GABA levels were associated with worsened symptoms of bradykinesia (slowed movement), rigidity (stiffness) and tremors. Since GABA is a chemical that blocks messages, lower levels of this means that messages are not being blocked and causing more frequent uncontrollable movements.

Reference:

van Nuland, A., den Ouden, H., Zach, H., Dirkx, M., van Asten, J., Scheenen, T., Toni, I., Cools, R., Helmich, R. (2019). GABAergic changes in the thalamocortical circuit in Parkinson’s Disease. Wiley, 41:1017-1029. https://onlinelibrary.wiley.com/doi/epdf/10.1002/hbm.24857