Maybe it's not the dopamine
Breakthrough in understanding the mechanism of Parkinson's disease
Anna Kerman, XX2 century, based on Medical News Today: Parkinson's breakthrough: New disease-causing mechanism found
The results of a new study conducted by scientists from South Korea and Singapore, "changed the idea that prevailed for thirty years" about the mechanism of occurrence of Parkinson's disease.
It is known that Parkinson's disease arises from a lack of the neurotransmitter dopamine. But it is still not known exactly what causes motor problems – including trembling, numbness and loss of control – which are signs of low dopamine levels.
It is known that arbitrary movements are controlled by basal nuclei. They alternately send signals that cause movement and suppress it. In order for the movements to be smooth, it is necessary to achieve an equilibrium between the two sets of signals. Since low levels of dopamine significantly interfere with movement (and is one of the main signs of Parkinson's disease), scientists have long been convinced that movement problems are caused by suppression due to a lack of dopamine.
The authors of the new study decided to use the latest technologies and test this assumption.
The leading co-authors of the work, Professor Kim Dae-su (Daesoo Kim) from the Department of Biological Sciences of the Korea Advanced Institute of Science & Technology, KAIST) in Daejeon, South Korea, and Professor George Augustine from Lee Kong Chian School of Medicine in Singapore, together with colleagues, applied a method called "optogenetics".
Using optogenetics, a method in which neurons are genetically modified to respond to light, the researchers amplified the signals of motor activity suppression. It turned out that the ventrolateral thalamic neurons involved in the control of motor function become hyperactive.
Apparently, this hyperactivity caused muscle rigidity and convulsions in the experimental rodents – symptoms that are the main signs of Parkinson's disease.
As the authors explain, this phenomenon is called a rebound, and it seems that it is caused by an increase in the suppressive signals of the basal nuclei.
Professor Kim and his colleagues conducted the following experiment to test their findings: for the experiment, they took mice that lacked dopamine as a result of genetic modifications. The phenomenon of ricochet was also suppressed: the rodents reduced the number of ventrolateral thalamic neurons.
To the surprise of scientists, mice with critically low levels of dopamine, but without rebound, moved normally and showed no signs of Parkinson's disease.
"With a low level of dopamine," the authors write, "the number of [ventrolateral thalamic] neurons exhibiting post–inhibitory activity increases, and the number of active [ventrolateral thalamic] neurons decreases due to the suppression of [basal nuclei] signals, which effectively prevents the motor symptoms of Parkinson's disease.
Consequently, the suppressive signals [of the basal nuclei] cause excitatory motor signals in the thalamus and additionally generate PD-like [Parkinson's disease-like] motor pathologies."
"The results of this study," says Professor Dae–soo Kim, commenting on the significance of the discovery, "completely change the ideas that have prevailed for thirty years about the causes of the development of symptoms of Parkinson's disease."
The first author of the work, Dr. Jeongjin Kim, says: "The discovery will have a huge impact on the treatment of Parkinson's disease. It may soon be possible to treat motor disorders without the use of levodopa, a precursor of dopamine."
"Our discovery is a real breakthrough in understanding how the brain controls body movements, and what goes wrong with Parkinson's disease and other disorders associated with a lack of dopamine," says Professor George Augustine.
The article Inhibitory Basal Ganglia Inputs Induce Excitatory Motor Signals in the Thalamus is published in the journal Neuron.
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