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Diabetes drug cuts Parkinson’s risk by 28%

A drug prescribed for diabetes patients reduces the risk of developing Parkinson’s disease by more than a quarter, a major study has found.

Researchers from the University of Bergen in Norway discovered glitazones (GTZs) had a protective effect against the degenerative neurological disease.

GTZs users saw a 28 percent drop in their chances of developing it compared with people on metformin, which is the most common medication for type 2 diabetes.

GTZs – also known as thiazolidinediones – are approved in the US and the UK for the metabolic disorder, but are not the primary treatment.

They are thought to work by helping the body to self-clean damaged or ageing brain cells.

Researchers believe glitazones (GTZs) may help prevent Parkinson’s by helping the body to ‘self-clean’ damaged or ageing brain cells (stock photo)

Previous studies have investigated their use for the prevention of Parkinson’s, but they have produced conflicting results.

Now scientists hope the findings of their analysis of more than 100 million drug prescriptions could lead to new way to prevent the devastating illness, which affects 10 million people worldwide.

The three main symptoms are involuntary shaking of particular parts of the body, slow movement and stiff and inflexible muscles.

There is no cure for the disease, and medication and brain stimulation can only alleviate symptoms.  

How the research was carried out

A study published in the journal PLOS Medicine in 2015 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],’ noted the study, which was published in the journal Movement Disorders.

And so a team from the University of Bergen in Norway analysed data from the Norwegian Prescription Database, which holds data on all medications dispensed in pharmacies across Norway, 

Over a 10-year period between January 2005 and December 2014, they identified 94,349 metformin users and 8,396 GTZ users who met the study criteria. 


Parkinson’s disease is caused by a loss of nerve cells in the part of the brain called the substantia nigra.

Nerve cells in this part of the brain are responsible for producing a chemical called dopamine. Dopamine acts as a messenger between the parts of the brain and nervous system that help control and co-ordinate body movements.

If these nerve cells die or become damaged, the amount of dopamine in the brain is reduced. This means the part of the brain controlling movement can’t work as well as normal.

The loss of nerve cells is a slow process. The symptoms of Parkinson’s disease usually only start to develop when around 80% of the nerve cells in the substantia nigra have been lost. 

It’s not known why the loss of nerve cells associated with Parkinson’s disease occurs, although research is ongoing to identify potential causes.

Exactly what causes the loss of nerve cells is unclear, but it’s thought genetic changes and environmental factors play a role.

Source: NHS Choices 

A ‘step toward solving the Parkinson’s riddle’ 

GTZs work in diabetics by increasing the body’s sensitivity to insulin, which is the hormone that regulates blood sugar levels. 

The researchers are unable to explain the precise mechanism behind why it may help to prevent Parkinson’s, but they speculate the drug might improve the function of mitochondria, which are known as the powerhouses of the cell. 

Through a process known as autophagy (‘self-eating’), cells digest their damaged or ageing mitochondria, clearing the way for healthy replacements. 

Research has shown issues with autophagy in people with Parkinson’s disease and Alzheimer’s disease.  

The team said 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,’ said study co-author Charalampos Tzoulis.

The scientists cite a number of limitations to their study. For instance, data was not available on the doses GTZ or metformin patients were taking. And there was a lack of information on the disease stage of each diabetic patient. 

Plus, because the study only included patients who had been diagnosed with diabetes, the findings cannot be generalized to the population as a whole.