Scientists are uncovering fresh evidence that exercise may help slow the progression of Parkinson's disease through biological signals released by muscles.
A review published in the journal Neuroprotection argues that exercise does more than improve strength, balance and mobility. It also stimulates the release of molecules known as "exerkines", which travel through the bloodstream and may reduce inflammation, protect nerve cells and support brain function. That raises new questions about whether health systems should place greater emphasis on physical activity as part of routine neurological care.
While researchers caution that much of the evidence remains preclinical, the findings point towards a growing understanding of how skeletal muscle communicates with the brain.
“We found that the exerkines act as a medium for the crosstalk between the muscle and the brain,” said the author of the study, Salomón Páez-García. “Though the brain controls muscles, exercising muscles send beneficial signals back to the brain through exerkines.”
Parkinson's disease affects more than 10 million people worldwide, and its prevalence is expected to continue rising as populations age. Existing medicines largely focus on controlling symptoms rather than slowing the underlying disease process, making lifestyle interventions an increasingly important area of research.
The findings also reinforce calls from patient groups for exercise to be treated as a core component of Parkinson's care rather than an optional extra. Although neurologists already recommend physical activity, dedicated rehabilitation services are often limited by workforce shortages and funding pressures.
Researchers are careful not to overstate the implications. The review concludes that much of the evidence for muscle-derived signalling molecules comes from laboratory and animal studies, and that large clinical trials are still needed to determine whether targeting these pathways can alter the course of Parkinson's disease in people.
“Exerkines are emerging as potential biomarkers and mediators of exercise-driven neuroprotection, but further high-quality studies are needed,” researchers said.