Parkinson’s doesn’t just affect movement and the brain—it may also impact the heart, according to new research from the University of Surrey. Scientists from Surrey’s School of Veterinary Medicine suggest that targeting a key protein outside of the brain could help manage Parkinson’s-related heart issues.

In a study published in Experimental Physiology, Surrey researchers studied mouse models and found a harmful buildup of the alpha-synuclein protein, which is associated with Parkinson’s disease, in a nerve cluster near the heart (the stellate ganglia). These nerves are part of the autonomic nervous system, which controls heart rate and rhythm.

Researchers found that 27% of neurons in the nerve cluster contained aggregated alpha-synuclein, forming similar toxic clumps seen in the brains of Parkinson’s patients. This finding suggests that Parkinson’s could disrupt heart function, not just movement and brain activity.

Professor Kamalan Jeevaratnam, lead author of the study and Head of the School of Veterinary Medicine at the University of Surrey, said, “Our study confirms the suspicion that there is a link between Parkinson’s disease and cardiac autonomic dysfunction—giving us a new insight into how the disease impacts the nervous system beyond the brain.

“And just like the brain, alpha-synuclein forms clumps in the nerves, strongly suggesting that the same process that damages brain cells in Parkinson’s is also damaging the nerves that control the heart.”

The research team used mouse models that produced a mutant form of alpha-synuclein. Then, using a precise dissection technique, they extracted the stellate ganglia, ensuring minimal tissue damage. The nerve clusters were then thinly sliced and stained with fluorescent markers, allowing scientists to track the spread and accumulation of the harmful protein within individual neurons.

Bonn Lee, a postgraduate student at the University of Surrey and co-author of the study, said, “Understanding how Parkinson’s affects the heart opens up new possibilities for treatment. If we can find ways to stop or slow the buildup of alpha-synuclein in the nervous system outside the brain, we could help manage some of the lesser-known but serious effects of the disease.

“We are keen to work with industrial partners on exploring whether targeting these toxic protein clumps in the heart’s nerve cells could improve symptoms and quality of life for people with Parkinson’s.”