Hannah Thomasy in The Scientist: For decades, researchers have appreciated the intimate association between mental health and physical health, and studies suggest that the mind may impact various bodily systems.1 For example, high levels of stress rendered people more vulnerable to infections; conversely, mental health treatment reduced the risk of rehospitalization by 75 percent in people hospitalized for heart disease.2,3
However, the mechanisms by which mental states might influence the immune or cardiovascular systems are still not well understood. Asya Rolls, a neuroscientist at the Technion – Israel Institute of Technology, said that these questions are often overlooked because many researchers feel that the field of mind-body connection is not amenable to rigorous scientific exploration. “It’s a major, fundamental gap in our understanding of physiology and medicine, and our ability to help patients,” she said.
Previously, Rolls has used mouse models to demonstrate how brain regions associated with reward or emotion can modulate immune activity and inflammation in various contexts, including infection, cancer, and colitis.4–6 As evidence of the association between mental health and cardiovascular disease in humans accumulated, she wondered if she might be able to mechanistically study this heart-brain connection in mice.7 Together with cardiovascular medicine specialist Lior Gepstein and Hevda Haykin, a jointly supervised graduate student, Rolls set out to explore how particular neural systems influenced recovery from acute myocardial infarction (AMI) in a mouse model.
In a recent study published in Nature Cardiovascular Research, the researchers found that chemogenetically stimulating dopaminergic neurons in the ventral tegmental area (VTA), part of the brain’s canonical reward circuitry, improved left ventricular ejection fraction (LVEF; a measurement of the heart’s ability to pump out blood), increased vascularization, and decreased fibrosis in the 15 days following AMI.8 This mouse model not only allowed researchers to objectively measure the effects of brain activity on heart function, but also to explore the mechanisms underlying these effects.
“We know that when we experience stress or happiness—things that we might think of as moods—it does have an impact on peripheral organs and peripheral immune cells,” said Isaac Chiu, a neuroimmunologist at Harvard Medical School who was not involved in the study. “So, I thought it was fascinating that they made a connection between the brain’s reward system and heart attacks.”
After two weeks of stimulating the VTA in the treatment group, said Rolls, “It was pretty interesting to see the changes between the groups. But the real challenge was to figure out how [this was happening].”
In previous research, she demonstrated that VTA activation altered immune responses, so they first examined immune cells present in the heart. They found reduced numbers of cells positive for CD68, a marker found on monocytes and macrophages. The significance of this finding is not entirely clear, however: CD68+ cells are diverse, and play complex and incompletely understood roles in both healing and detrimental changes to the structure of the heart after AMI.9
More here.
