Researchers have found that a type of asthma drug may halve a patient's risk of developing Parkinson's disease -- a chronic disease with unknown causes.
The disease destroys the brain cells that control body movements. Shivering, stiff arms and legs and poor coordination are typical symptoms of Parkinson's. The symptoms may develop slowly, and it sometimes takes time to make a correct diagnosis.
The findings, published in the journal Science, could lead to new treatment of Parkinson's patients.
"Our discoveries may be the start of a totally new possible treatment for this serious disease. We expect that clinical studies will follow these discoveries," said Trond Riise, Professor at Department of Global Public Health and Primary Care (IGS), University of Bergen in Norway.
Examining the pharmaceutical history of more than four million Norwegians over an 11-year period, the researchers found that Beta2-adrenoreceptor agonists may reduce Parkinson's disease.
The medicine regulates expression of levels of SNCA gene linked to Parkinson's disease risk, the study said.
For the study, the researchers examined more than 100 million Norwegian prescriptions registered since 2004.
"Our analysis of data from the whole Norwegian population has been decisive for the conclusion in this study," Riise said.
In the study, the treatment of Parkinson's was linked to prescriptions of asthma medicine and the medicine for high blood pressure.
The Norwegian analysis was done after researchers at Harvard University found these effects of the medicines in animal tests and in experiments with brain cells in the lab.
To find out if these medicines had the same effect on humans, the researchers at Harvard University started to collaborate with the Norwegian research team.
"We analysed the whole Norwegian population and found the same results as in the animal testing at Harvard University. These medicines have never been studied in relation to Parkinson's disease," Riise said.
--IANS
gb/vt
Disclaimer: No Business Standard Journalist was involved in creation of this content
