Research teams at Harvard University in Cambridge, Massachusetts, and the University of Bergen in Norway have collaborated to study a thousand different drugs and their effect on the risk of Parkinson’s disease.
New Research on Parkinson’s Treatments
The findings of a study authored by Harvard University’s Shuchi Mittal were published in the journal Science. The experiments involved studying the effect of a large number of drugs on the risk of Parkinson’s disease. Parkinson’s is associated with the build-up of a brain protein known as alpha-synuclein. Excess clumps of the protein lead to Parkinson’s symptoms. The investigators used cell cultures to identify compounds that down-regulate the protein-forming gene. Small molecule screening revealed that beta-2-adrenoreceptor agonists can potentially reduce the expression of the gene that leads to the formation of alpha-synuclein.
Asthma Drugs May Lower Parkinson’s Risk
Two types of beta-2-adrenoreceptor agonists were tested in mice. Salbutamol (an asthma drug) and beta blockers (medications used to treat hypertension) are both beta-2-adrenergic agonists. Mittal and her team examined 100 million prescriptions from a Norwegian database over a period of more than 10 years. Co-author of the study, Professor Trond Riise, explains that the results in the Norwegian population mirrored the findings in the laboratory animals at Harvard.
The study showed that asthma drugs such as salbutamol reduce the risk of Parkinson’s by more than 30 percent. On the other hand, hypertension medicine propranolol increases the risk of Parkinson’s by two times. This is the first time these drugs were studied for their effect on risk of Parkinson’s disease. Further clinical studies will determine whether new treatments for Parkinson’s are possible.
Do Beta Blockers Cause Parkinson’s Disease?
The research team cautions that an association between a drug and Parkinson’s does not imply that the medication causes the disease. The increased risk of Parkinson’s could be due to alpha-synuclein accumulation because beta blockers might increase the expression of the gene through acetylation. In contrast, asthma medications promote neuron health by decreasing the expression of the gene through deacetylation. The disease in its early stages is characterized by mitochondrial dysfunction in nigral dopamine neurons.
The findings are significant as they point to a potential new drug strategy for Parkinson’s disease, says Dr. Clemens Scherzer, principal investigator and neurologist at Harvard Medical School’s Ann Romney Center for Neurologic Diseases.