It’s well known that having an optimistic view brings mental well-being, which then trickles down to positively affect other parts of the body. Studies have shown that people who approach life in this way are more likely to have healthy hearts and thus live longer. But what makes this connection? A new study from Johns Hopkins University School of Medicine has found that there’s a single protein responsible for regulating both the mind and the heart.

The protein is called brain-derived neurotrophic factor (BDNF), and it’s responsible for the survival, growth, and maintenance of nerve cells. BDNF is active at neurons’ synapses — where cells communicate with each other — and it plays a role in synaptic plasticity, or the ability of these synapses to become stronger, promoting learning and memory. In addition to all that, the protein has also been shown to act as a natural antidepressant and nourish blood vessels.

A research team led by Dr. Ning Feng, a cardiology fellow at the School of Medicine, found in both mice and lab-grown heart cells that BDNF’s responsibilities span further than the brain to help keep the heart beating properly. Specifically, it’s part of a number of other chemical processes that maintain the heart’s rhythm and strength, allowing it to contract and relax.

“Our results are not only a vivid reminder of the astounding complexity of the heart’s chemistry and physiology, but also a striking example of the ability of a single protein to act on multiple fronts, and affect many organs and functions,” Feng said in a press release.

For the study, the researchers looked at how BDNF affected both healthy and failing heart cells from mice. They found that healthy hearts responded strongly by contracting and relaxing, while the failing hearts responded weakly or not at all. The reason for this, the team found, was that normal hearts had a different version of BDNF’s receptor molecular TrkB than the failing hearts. TrkB resides on the surface of cells, and triggers a catalyst protein that signals BDNF activity within the cell, but among the failing hearts, that catalyst protein was less active. Mice engineered to lack TrkB receptors eventually developed impaired heart function. The researchers said this variation in TrkB is fairly common and having it doesn’t necessarily mean that person will develop disease; they just might not be as capable of utilizing BDNF.

“Taken together, these findings show that any abnormality in the way BDNF communicates with its receptor appears to unlock a cascade of chemical glitches that eventually leads to poor cardiac function,” Feng said. This ability for BDNF to move from the brain to the heart, and nurture both organs’ functions, suggests a possible biochemical link between depression and heart disease, the researchers said. After all, if the naturally antidepressant protein glitches in the heart, there’s a good chance it can glitch in the brain, too.

But taking that a step further, there’s a chance it could also explain the possible link between dementia and heart disease. Studies have shown a link between irregular heartbeats and atherosclerosis — a buildup of plaque in the arteries — and cognitive decline. And the Alzheimer’s Association says, “Some of the strongest evidence about maintaining your brain links brain health to heart health. … If your heart isn’t pumping well — or if your brain’s blood vessels are damaged — your brain cells have trouble getting all the food and oxygen they need.”

While its connection to dementia and depression are only speculative, the researchers believe the study results show that people with BDNF insensitivity, or a lack of the protein altogether, may be at risk of heart failure. “Just like a constant low flame can keep a pot on slow simmer, constant levels of BDNF seem to maintain heart muscle vitality,” said Dr. Nazareno Paolocci, assistant professor of medicine at the School of Medicine, in the release. Even “in the absence of chronic stressors, such as hypertension or an elevated workload of the heart muscle, BDNF deficiency may not cause full-blown disease, but it could be the proverbial straw that leads to a ‘broken heart.’”

Source: Paolocci N, Feng N, Huke S, et al. PNAS. 2015.