华盛顿大学医学院和普林斯顿大学研究人员发现，儿童期严重压力会通过改变脑细胞DNA的包装方式，在脑细胞内留下持久的生物学印记1。研究表明，应激会导致SETD7酶在脑细胞中水平升高，该酶通过添加H3K4me1标记使DNA结构变得更加开放，从而使压力反应基因更容易被激活1。研究人员成功通过阻断SETD7的作用，保护小鼠免受长期压力敏感性的影响1。
这项研究聚焦于腹侧被盖区（VTA），该区域含有产生多巴胺的神经元1。全球超过一半的儿童经历过某种形式的早期生活压力，经历四种或更多不利事件与后期身心健康问题风险显著升高相关1。研究团队负责人Meaghan Creed博士表示："我们发现了一个新的生物学过程，将早期逆境经历与长期心理疾病易感性联系起来"1。另一位研究人员Catherine Jensen Peña博士指出："目前没有针对早期生活压力对大脑影响的治疗方法"1。该研究发表于2026年8月7日《Neuron》杂志1。
Researchers from Washington University School of Medicine and Princeton University have identified a biological mechanism through which severe stress during childhood creates persistent changes in brain cells.1 The study found that early-life adversity alters how DNA is packaged within neurons, making stress-response genes more easily activated throughout a person's lifetime.1
The research, published in Neuron on August 7, 2026, focused on the ventral tegmental area of the brain, a region containing dopamine-producing neurons.1 Scientists discovered that in stressed mice, levels of the SETD7 enzyme increased, adding chemical markers called H3K4me1 to DNA that opened up its structure.1 By blocking the action of SETD7 and preventing these markers from being added, researchers successfully protected mice from developing long-term stress sensitivity.1
The findings address a significant public health concern: more than half of children globally experience some form of early-life stress, and those exposed to four or more adverse events face substantially elevated risks of mental and physical health problems later in life.1 According to Dr. Meaghan Creed, "We discovered a novel biological process linking early adversity experiences to long-term vulnerability to mental illness."1 Dr. Catherine Jensen Peña added, "Currently there are no treatments targeting how early-life stress affects the brain," underscoring the potential clinical importance of this discovery.1
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