This study investigated how severe stress during childhood may produce long-lasting changes in the brain, increasing vulnerability to anxiety, depression and other mood disorders later in life. Researchers from Washington University School of Medicine and Princeton University found a possible biological mechanism explaining this effect.

The research focused on the ventral tegmental area (VTA), a brain region containing dopamine-producing neurons involved in processing reward and stressful experiences. The researchers examined changes to the epigenome, which consists of molecular mechanisms that influence whether genes are switched on or off without changing the DNA sequence itself.

In young mice exposed to early-life stress, researchers found increased levels of an enzyme called SETD7. This enzyme adds a molecular marker that makes DNA packaging more open. As a result, stress-related genes become easier to activate, potentially making the brain more sensitive to future stressful experiences.

When researchers increased SETD7 in young mice that had not experienced early stress, the mice later showed more reactive dopamine neurons and greater anxiety-like behaviour. However, reducing SETD7 activity after early stress appeared to protect the mice from becoming unusually sensitive to stress later in life.

The findings suggest that early adversity may leave a lasting epigenetic “molecular scar” that affects how the brain responds to future stress. However, as the study was conducted using mice, further research is needed to establish whether the same mechanisms occur in humans. The research may eventually help scientists develop treatments or supportive interventions to reduce the long-term effects of childhood trauma.

https://www.sciencedaily.com/r...

1. What role does the epigenome play in the effects of early-life stress?

2. Why did the researchers focus on the ventral tegmental area (VTA)?

3. What is one limitation when applying the findings of this study to humans?