Recently, a new study held by scientists from both South Korea and Singapore could potentially revoke decades of consensus and agreement on the reasons for symptoms of Parkinson’s disease. The study can be seen here. If you are wondering what is Parkinson, you can find out really quickly here where we did a quick summary on the disease. The research was co-led by Daesoon Kim from the Korea Advanced Institute of Science & Technology, and George Augustine, from the Lee Kong Chian School of Medicine.
Potential breakthrough in Parkinson’s disease, new disease causing mechanism found
Going into the technical and scientific details, the progression of the disease is usually correlated with the increasingly depleting levels of the neurotransmitter known as dopamine. However, strictly speaking, scientists and researchers have not been able to point to exact causes on why there are issues of motor problems associated with a low level of dopamine.
Voluntary body movement is postulated to be controlled by an area in the brain known as basal ganglia. From this area of the brain, instructions which both drive activity and suppress body movements are issued, alternating between motion and suppression. Achieving a delicate equilibrium between the two sets of differing instructions will allow smooth motion. It is commonly believed that a low level of dopamine is associated with the progression of Parkinson as cases observed often show inactivity with a regressing level of dopamine. This belief is now potentially untrue.
High technology study method resulted in significant findings
Through the use of the procedure known as optogenetics, the researchers wanted to gauge how genetically modified neurons would respond to light, which makes it much more feasible for them to monitor and supervise the way the cells behave. They subsequently found that by issuing the set of instructions which ask the cells to stop themselves in action, this actually resulted in higher activity for motor control, sparked off by the ventrolateral thalamic neurons. This phenomenon of higher activity actually appeared to cause rigidity in muscle movements for rodents, somewhat similar to how patients suffering from Parkinson’s disease will experience a degree of muscle contractions.
How was the theory being tested and validated?
Eventually, the researchers tested their hypothesis by genetically engineering mice to have a low level of dopamine and stopping reflex actions control to observe the effects it have on symptoms very similar to Parkinson. Unexpectedly, mice with a surprisingly low level of dopamine, and restricted hyperactivity in the ventrolateral thalamic neurons displayed usual movement patterns and no symptoms similar to Parkinson’s disease.
This means that all the past research about how a low level of dopamine might be the cause of Parkinson could be untrue. Rather, it could be that the body’s response to a high degree of hyperactivity in the ventrolateral thalamic neurons which are involved in motor control causing Parkinson like symptoms, and is thought to be triggered by inhibiting basal ganglia inputs.
The technical details for this paper is quite complicated, and I spent significant time understanding and rewording it in a way which makes it relatively simpler. The findings are claimed to be a breakthrough, and we are able to see how control over the human body can be affected by parts of the brain which send certain signals regulating normal body activity. These signals, when overly excited can cause Parkinson like symptoms.
The implications for future treatments and cures could be interesting, which brings me to my next point. Are the current treatments then invalid in the light of these new findings? What are the responses from the medical community to this paper and are prescription of the usual medical treatment drugs for Parkinson still ongoing?
In a perfect market with perfect knowledge, the demand for certain drugs might fall depending on information released. Unfortunately, the findings are novel, but there does not seem to be an alternative in the short term.