This natural antidepressant protein can help sustain sound mind, strong heart
A protein, called BDNF (brain-derived neurotrophic factor), already known to act as a natural antidepressant, can help sustain sound mind and strong heart.
Washington: A protein, called BDNF (brain-derived neurotrophic factor), already known to act as a natural antidepressant, can help sustain sound mind and strong heart.
The team's experiments, conducted in mice and lab-grown heart cells, show this multi-tasking protein, which can enhance learning and memory, power nerve cell growth, and nourish blood vessels also helps sustaining the ability of heart muscle cells to contract and relax properly.
The results revealed that either BDNF deficiency or cell insensitivity to BDNF's presence can precipitate heart muscle dysfunction, particularly under conditions of chronic or repeated physical stress on the heart, such as endurance training or high blood pressure.
Specifically, the researchers tracked BDNF's role in a cascade of molecular signaling events in heart cells, the disruption of which led to heart muscle failure.
If confirmed in humans, the research team said, the findings could pave the way to new treatments for certain forms of heart failure, a disorder that affects nearly 6 million Americans and more than 23 million people worldwide.
In addition, because of BDNF's well-known antidepressant effects and its role as a booster of nerve cell health, the research teams says the results suggested that a possible biochemical link between depression and heart disease, two disorders that tend to occur in concert but whose relationship remains poorly understood.
The findings also can help clarify the biological means behind recent, and unexplained observations, that heart failure patients whose cardiac function worsens during physical exertion have low levels of BDNF in the blood.
The researchers point out that low level of BDNF by themselves may not be enough to cause immediate heart disease, but chronic BDNF deficiency or insensitivity, compounded by additional physiologic or pathologic stressors, was a main culprit in fueling the disease.
The research is published in the Proceedings of the National Academy of Sciences.