Scientists in South Korea and Singapore are overturning three decades’ worth of knowledge about Parkinson’s and what causes it.
Up until now, scientists have thought that the cause of the lack of voluntary movement (which is one of the biggest characteristics of Parkinson’s) is low levels of dopamine. However, this no longer seems to be the case.
The basal ganglia regulates the body’s voluntary movement. This region of the brain basically shifts between getting instructions to allow movement, and getting instructions to suppress movement.
Well, researchers Daesoo Kim (South Korea) and George Augustine (Singapore) made use of the cutting-edge technology optogenetics to intensify the motor suppression instructions given to rats’ brains.
As Medical News Today states:
“However, they found that this made ventrolateral thalamic neurons – which are involved in motor control – hyperactive.
This hyperactivity seemed to cause muscular rigidity and contractions in the rodents – symptoms similar to the hallmark motor symptoms in Parkinson’s disease.
As the authors explain, this is the phenomenon called “rebound firing,” which seems to be triggered by intensifying inhibitory basal ganglia inputs.
Prof. Kim and team tested the role of this phenomenon by genetically engineering mice to lack dopamine and inhibiting rebound firing to see what effects it would have on Parkinson’s disease motor symptoms.
Rebound firing was inhibited by genetically interfering to reduce the number of ventrolateral thalamic neurons.”
SHOCKINGLY, THE MICE WITH EXTREMELY LOW LEVELS OF DOPAMINE – BUT NO REBOUND FIRING – SHOWED NO SYMPTOMS OF PARKINSON’S.
According to Kim and Augustine:
“In a low dopamine state,” the authors say, “the number of [ventrolateral thalamic] neurons showing post-inhibitory firing increases, while reducing the number of active [ventrolateral thalamic] neurons [by inhibiting basal ganglia] input, effectively prevents Parkinson disease-like motor symptoms.”
“Thus, [basal ganglia] inhibitory input generates excitatory motor signals in the thalamus and, in excess, promotes PD-like [Parkinson’s disease-like] motor abnormalities,” they conclude.
“THIS STUDY,” SAYS PROF. DAESOO KIM, AS HE COMMENTS ON THE SIGNIFICANCE OF THE FINDINGS, “OVERTURNS THREE DECADES OF CONSENSUS ON THE PROVENANCE OF PARKINSONIAN SYMPTOMS.”
First study author Dr. Jeongjin Kim says, “The therapeutic implications of this study for the treatment of Parkinsonian symptoms are profound. It may soon become possible to remedy movement disorders without using L-Dopa, a precursor to dopamine.”
These findings offer significant breakthroughs in the understanding of Parkinson’s disease and the way it comes to form in the body.
Through this study, researchers now have a far greater understanding of how the brain typically controls the body’s movement, and how Parkinson’s disease affects this control.