Exercise slows the progression of Parkinson’s disease

Exercise slows the progression of a harmful protein in the brain believed to contribute to the degenerative disease Parkinson’s, a new study revealed.

New research has uncovered the molecular reasons behind the link between exercise and the disease that has remained a mystery until now.

Researchers discovered that running on a treadmill can stop the accumulation of a protein in brain cells called alpha-synuclein, which they believe plays a central role in brain cell death.

The findings suggest that exercising can help stop Parkinson’s in its tracks, as the disease is incurable, affecting 60,000 Americans a year. 

Exercise stops the progression of a protein in the brain that is produced in Parkinson’s patients, according to researchers from the University of Colorado

Scientists from the University of Colorado tested mice who started developing Parkinson’s symptoms in mid-life, as humans do. 

Running wheels were then put into their cages at 12 months old.

After three months, the mice that ran showed improved movement and cognitive function compared to the group of mice that did not run. 

The results published in the journal PLOS ONE found that exercise increased brain and muscle expression of a key protective gene called DJ-1. 

Though rare, humans born with a mutation that mutes the helpful DJ-1 gene are guaranteed to get severe Parkinson’s at a relatively young age.

‘Our results indicate that exercise may slow the progression of Parkinson’s disease by turning on the protective gene DJ-1 and thereby preventing abnormal protein accumulation in brain,’ said study author Dr Curt Freed.


About 60,000 Americans are diagnosed with Parkinson’s and there are around one million sufferers in the US.

It causes muscle stiffness, slowness of movement, tremors, sleep disturbance, chronic fatigue, an impaired quality of life and can lead to severe disability. 

It is a progressive neurological condition that destroys cells in the part of the brain that controls movement. 

Sufferers are known to have diminished supplies of dopamine because nerve cells that make it have died.

There is currently no cure and no way of stopping the progression of the disease, but the new findings offer hope.

The researchers tested mice that were missing the DJ-1 gene and discovered that their ability to run had severely declined, suggesting that the DJ-1 protein is required for normal movement.

Freed explained that the animal experiments have significant implications for humans.

‘Our experiments show that exercise can get to the heart of the problem in Parkinson’s disease,’ Freed said. 

‘People with Parkinson’s who exercise are likely able to keep their brain cells from dying,’ he added.

Parkinson’s is a disease caused by the death of brain cells that make a critical neurotransmitter called dopamine. 

The loss of dopanine in the brain makes voluntary movement impossible.  

The disease causes muscle stiffness, slowness of movement, tremors, sleep disturbance, chronic fatigue, an impaired quality of life and can lead to severe disability. 

Most people with Parkinson’s disease take a drug called L-DOPA to treat their symptoms. 

That drug is converted into dopamine, allowing patients to move.

In 1988, Freed and his colleague Dr Robert Breeze performed the first transplant of human fetal dopamine cells into a Parkinson’s patient in the United States. 

His lab is currently working to convert human embryonic stem cells to dopamine neurons. 

These techniques should make it possible to produce unlimited quantities of dopamine cells for transplant.


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