Parkinson’s disease is most widely known for causing muscle tremors and motor-control symptoms, but most Parkinson’s sufferers also exhibit damage to their hearts’ connection to the sympathetic nervous system. In fact, that damage is one of the first signs of Parkinson’s, but the connection is often not made until the more visible symptoms develop.

Researchers at the Wisconsin National Primate Research Center (WiNPRC) and the University of Wisconsin (UW-Madison) have found a new way to examine stress and inflammation in the heart that could serve as an early indicator of Parkinson’s well before the more common symptoms begin.

The heart damage is significant because it contributes to a tendency for Parkinson’s patients to suffer physical injury as a result of blood pressure fluctuations.

“This neural degeneration in the heart means patients’ bodies are less prepared to respond to stress and to simple changes like standing up,” said Marina Emborg, a University of Wisconsin–Madison professor of medical physics and Parkinson’s researcher at the WiNPRC. “They have increased risk for fatigue, fainting and falling that can cause injury and complicate other symptoms of the disease.”

The sympathetic nervous system signals the heart to accelerate its pumping to match quick changes in activity and blood pressure. Researchers at WiNPRC developed a method for tracking the mechanisms that cause the damage to heart nerve cells, then tested the method in the nervous system and heart of monkeys.

Ten rhesus macaque monkeys served as models for Parkinson’s symptoms, receiving doses of a neurotoxin that caused damage to the nerves in their hearts in much the same way Parkinson’s affects human patients. Once before and twice in the weeks after, the monkeys underwent PET scans, a medical imaging technology that can track chemical processes in the body using radioactive tracers.

The UW–Madison researchers used three different tracers to map three different things in the left ventricle of the monkeys’ hearts: where the nerves extending into the heart muscle were damaged, where the heart tissue was experiencing the most inflammation, and where they found the most oxidative stress.

The scans were accurate enough to allow the researchers to focus on changes over time in specific areas of the heart’s left ventricle.

“We know there is damage in the heart in Parkinson’s, but we haven’t been able to look at exactly what’s causing it,” said researcher Jeannette Metzger. “Now we can visualize in detail where inflammation and oxidative stress are happening in the heart, and how that relates to how Parkinson’s patients lose those connections in the heart.”

By tracing the progression of nerve damage and its potential causes, the radioligands can also be used to test potential new treatments. The researchers gave half the monkeys in the study a drug, pioglitazone, that has shown promise in protecting central nervous system cells from inflammation and oxidative stress.

“The recovery of nerve function is much greater in the pioglitazone-treated animals,” added Emborg. “And what’s interesting is this method allows us to identify very specifically the differences the treatment made—separately for inflammation and for oxidative stress—across the heart.”

The heart problems opened to examination by the new imaging methods are not limited to Parkinson’s disease. Heart attacks, diabetes and other disorders cause similar damage to nerves in the heart, and those patients and potential therapies could also benefit from the new visualization method.

The results suggest human patients could benefit from the radioligand scans, and Metzger wonders if it could help catch some Parkinson’s patients before their other symptoms progress.