Latest research on the causes of Parkinson’s disease has led to the discovery of a key factor responsible for the damage of the brain cells.
The paper was published in the latest Journal of Immunology which describes the region of the brain that is controlled by this causal factor of Parkinson’s disease.
The research was conducted by scientists at the Scripps Research Institute, La Jolla, California, under the guidance of lead author Bruno Conti.
What is Parkinson’s disease
Parkinson’s disease is one of the leading neurological diseases afflicting many aged people around the world. The main symptom of the disease is the loss of motor control and coordination due to reduction in the number of nerve cells (neurons) in the mid brain called Substantia Nigra.
In majority of the cases, the origin of the disease is unknown, but now some neuro-inflammation mediators are considered to be involved in damaging the dopamine-generating neurons.
Study and Research in Mouse Models
Conti and his research team used data from human genomics to pinpoint the exact biological pathways involved in the immune response to damage of the dopaminergic neurons. During this process they discovered a protein called IL-13Ra1 located in the PARK 12 locus of the genomic sequence. This they found was involved in Parkinson’s disease. The protein is actually a receptor chain that mediates the action of 2 cytokines –IL-13 & IL-14 (also involved in the immune responses to allergic reactions).
The study was conducted on mice and it was found that the protein receptor IL-13Ra1 is present only on the surface of dopaminergic neurons. The long term experiment on mice which suffered from symptoms similar to that of Parkinson’s. The mice were determined for the presence or lack of the IL-13Ra1 and then measured the specific neuron density in the region of interest.
The scientists felt that knocking off this receptor would trigger more inflammation and hasten the process of neural cell loss. But to their surprise they found that the situation improved. The neuron count got better. This means that the cells did better in the absence of the receptor.
Then they unearthed a basic mechanism that showed preferential loss of the neurons when neuroinflammation happened together with oxidative stress. The study also suggested that anti-inflammatory cytokines may be contributing to neuron loss. Thus they feel that the IL-14 pathway is the main player in Parkinson’s disease. The scientists also suggest that since IL-13 plays a major role in allergic inflammation pathway and thus allergic individuals may be more prone to Parkinson’s than the others.
Relevance of This Research
The results in mice might be replicated in humans too. The challenge for the researchers then lies in proving it. If this turns out as expected, then the results will pave way for better understanding of the cause of Parkinson’s and help provide a definitive drug based on the IL-13 and Il-14 pathways.
