https://www.eurekalert.org/pub_releases/2021-03/tmsh-emc031021.php
News Release 15-Mar-2021
The Mount Sinai Hospital / Mount Sinai School of Medicine
An epigenetic modification that occurs in a major cell type in the brain's reward circuitry controls how stress early in life increases susceptibility to additional stress in adulthood, researchers at the Icahn School of Medicine at Mount Sinai have learned. In a study in Nature Neuroscience, the team also reported that a small-molecule inhibitor of the enzyme responsible for this modification, currently being developed as an anti-cancer drug, was able to reverse increased vulnerability to lifelong stress in animal models.
"It has long been known that stress exposures throughout life control lifelong susceptibility to subsequent stress. Here we discovered a key molecular mechanism that mediates the lasting effects of that stress," says lead author Hope Kronman, an MD, PhD student in the Nash Family Department of Neuroscience and The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai.
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A lifelong history of stress is the strongest known risk factor for depression in humans. Previous studies have shown that early-life stress increases the risk of adult depression as much as threefold, depending on its timing, intensity, and specific features. Early-life stress is also known to increase the likelihood of behavioral susceptibility to stress later in life, and to have particularly strong effects on the nucleus accumbens, an essential component of the brain's reward system.
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