A class of drugs currently used to treat diabetes could lower the risk of developing Parkinson’s, a new study reveals, offering hope of new prevention and treatment strategies for the disease.
By analyzing more than 100 million drug prescriptions in Norway, researchers found that patients who used glitazones (GTZs) saw their risk of Parkinson’s disease reduced by more than a quarter.
GTZs – also known as thiazolidinediones – are approved in the United States for the treatment of type 2 diabetes. They work by increasing the body’s sensitivity to insulin, which is the hormone that regulates blood sugar levels.
Study co-author Charalampos Tzoulis, from the University of Bergen in Norway, and colleagues recently reported their results in the journal Movement Disorders.
Studies have investigated the use of GTZs for the prevention of Parkinson’s disease, but they have produced conflicting results. A study published in the journal PLOS Medicine in 2015, for example, identified a lower incidence of Parkinson’s in patients who used GTZs, while another found no link between GTZ use and Parkinson’s risk.
“Based on current evidence, it remains unclear whether GTZs have a neuroprotective effect in PD [Parkinson’s disease],” note Tzoulis and colleagues.
Aiming to gain a better understanding of the link between GTZ use and Parkinson’s risk, the researchers analyzed data from the Norwegian Prescription Database, which holds data on all medications dispensed in pharmacies across Norway, as well as information on the patients to whom these medications are prescribed.
The researchers looked at the link between the use of GTZs, metformin – which is the primary drug prescribed for type 2 diabetes – and the development of Parkinson’s disease.
Over a 10-year period between January 2005 and December 2014, the team identified 94,349 metformin users and 8,396 GTZ users who met the study criteria.
The study revealed that, compared with users of metformin, patients who used GTZs were 28 percent less likely to develop Parkinson’s disease.
They are unable to explain the precise mechanisms behind their findings, but they speculate that GTZs might improve the function of mitochondria. These are organelles that produce energy for cells, enabling them to function.
In a previous study, Tzoulis and team found that patients with Parkinson’s disease experience a reduction in mitochondrial production. “It is possible,” they say, “that GTZ drugs ameliorate these defects by increasing mtDNA [mitochondrial DNA] synthesis and overall mitochondrial mass.”
Still, the team says that further studies are needed to investigate this possible mechanism. “If we understand the mechanisms behind the protection, then we have a chance to develop a new treatment,” says Tzoulis.
The researchers cite a number of limitations to their study. For instance, the team did not have data on the GTZ or metformin dose each patient was using, so they are unable to determine the dose-response relationship between diabetes medication and the risk of Parkinson’s disease.
Also, the researchers note the lack of information on the diabetes stage of each patient. “However,” they say, “as diabetes has not been shown to have a definite effect on the risk for PD, we find it unlikely that treatment stage would significantly bias our results.”
Because the study only included patients who had been diagnosed with diabetes, the findings cannot be generalized to the population as a whole.
That said, the team believes that the study could lead to new prevention and treatment strategies for Parkinson’s disease, a condition that is diagnosed in around 60,000 people in the U.S. every year.
“We have made an important discovery, which takes us a step further toward solving the Parkinson’s riddle.”