According to a pilot study by Yale School of Medicine, exercise doesn’t just slow down the neurodegeneration associated with Parkinson’s Disease, there is evidence it can reverse it

Parkinson’s disease is the most increasingly prevalent neurological disorder and it’s estimated it will impact 12 million people by 2040.

The disease has no cure – only medication and therapy to treat the symptoms – however, a new study by Yale University suggests exercise could help to mitigate the enormous personal and economic costs the disease presents.

Two previous clinical trials have shown that engaging in high-intensity exercise, three times a week for six months, is correlated with less severe motor symptoms. However, the Yale study goes one step further, using brain scans for the first time to find evidence of further health benefits.

Protecting the neurons
Parkinson’s disease is caused by the misfolding of Alpha-synuclein, a protein, which accumulates within neurons and damages them. As the cells die, the lack of dopamine creates the physical symptoms, particularly motor tremors and slowed movements.

“By the time patients clinically manifest the typical motor symptoms of Parkinson’s, you can assume that the neurodegenerative process actually started much earlier, maybe a decade or two,” says Sue Tinaz, associate professor of neurology and co-principal investigator.

The most common available medication replaces the dopamine, which alleviates the symptoms but doesn’t prevent the ongoing neurodegeneration. Long-term use can also cause undesirable side-effects, such as uncontrolled, excessive movements.

However, high-intensity aerobic exercise has been shown to preserve the neurons that produce dopamine – the chemical in the brain that helps cells communicate. These brain cells are the most vulnerable to destruction in patients with Parkinson’s disease.

Remarkable results
Yale’s proof-of-concept study involved 10 patients who had been diagnosed for less than four years and had not lost all their dopamine-producing neurons. At the start of the trial they received MRI and PET scans to measure the amount of neuromelanin found in dopamine-producing neurons and the protein dopamine transporter (DAT) which helps the neurons maintain proper dopamine levels.

After six months of HIIT three times a week, the brain imaging scans showed a significant increase in both the neuromelanin and DAT signals in the substantia nigra. Researchers say this suggests high-intensity exercise not only slowed down the neurodegenerative process but help the dopaminergic system grow healthier.

“Where we would have ordinarily expected to see a decline in the DAT and neuromelanin signals, we saw an increase,” says Bart de Laat, the study’s first author. “We had hoped to see that the neurodegeneration would not progress as quickly or stop temporarily, but instead we saw an increase in nine out of 10 people.”

Tinaz says the study highlights the importance of including an exercise regimen as part of a Parkinson’s treatment plan: “Available medications are only for symptomatic treatment and do not change the disease course. “But exercise seems to protect the brain at the neuronal level.”

More: www.medicine.yale.edu