Scientists are building a stronger case that exercise could become a standard part of Parkinson's disease treatment, not just for its physical benefits but because of the biological signals it sends from muscles to the brain. A review published in the journal Neuroprotection argues that physical activity stimulates the release of molecules called exerkines, which travel through the bloodstream and may reduce inflammation, protect nerve cells, and support brain function.
The review, led by Salomón Páez-García, synthesises evidence from laboratory and animal studies to explain 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,” Páez-García said. “Though the brain controls muscles, exercising muscles send beneficial signals back to the brain through exerkines.”
Beyond strength and balance
Parkinson's disease affects more than 10 million people worldwide, and its prevalence is expected to rise as populations age across Europe and beyond. Existing medications primarily manage symptoms such as tremors, stiffness, and slowness of movement, but they do little to slow the underlying neurodegenerative process. That gap has made lifestyle interventions—especially exercise—an increasingly important area of research.
The findings reinforce calls from patient advocacy groups across the continent to treat exercise as a core component of Parkinson's care rather than an optional extra. Neurologists in many European countries already recommend physical activity, but dedicated rehabilitation services are often constrained by workforce shortages and funding pressures. In Germany, for example, specialised physiotherapy for Parkinson's is unevenly available, while in the UK, the National Health Service has faced criticism for inconsistent access to neurological rehabilitation.
Researchers are careful not to overstate the implications. The review concludes that much of the evidence for muscle-derived signalling molecules comes from preclinical models, and that large clinical trials are still needed to determine whether targeting these pathways can alter the course of Parkinson's disease in humans. “Exerkines are emerging as potential biomarkers and mediators of exercise-driven neuroprotection, but further high-quality studies are needed,” the researchers noted.
Still, the concept has captured attention in the medical community. If exerkines can be reliably measured, they might one day serve as biomarkers to monitor disease progression or to tailor exercise prescriptions for individual patients. That could have practical implications for how health systems design rehabilitation programmes, potentially shifting resources from purely pharmacological approaches to integrated care that includes structured physical activity.
Across Europe, initiatives are already exploring this direction. In the Netherlands, the Parkinsondans project combines dance and exercise classes, while in Sweden, researchers are testing high-intensity interval training in clinical settings. These efforts align with the growing recognition that muscle–brain communication is a two-way street, and that exercise may offer a low-cost, accessible complement to drug therapy.
The review also touches on the broader potential of exerkines beyond Parkinson's, including possible applications in other neurodegenerative conditions such as Alzheimer's disease. However, the authors stress that the field is still young, and that translating laboratory findings into clinical practice will require rigorous investigation.
For now, the message to patients and clinicians is pragmatic: exercise is safe, beneficial for overall health, and may have neuroprotective effects that extend beyond what was previously understood. As the evidence matures, it could reshape guidelines for Parkinson's management across Europe, making physical activity a pillar of care rather than an afterthought.
