这项在美国圣路易斯开展的研究由华盛顿大学医学院与普林斯顿大学共同完成，论文于2026年8月7日发表在《Neuron》期刊 1。科研团队发现，童年早期压力会通过改变大脑多巴胺神经元中DNA的包装方式，在成年后留下对压力更敏感的“分子疤痕” 1。该研究聚焦于腹侧被盖区产生多巴胺的神经元 1。
机制研究表明，童年压力会导致酶SETD7水平升高，增加DNA包装上的H3K4me1化学标记 1。H3K4me1标记使DNA结构更开放，压力相关基因更易激活 1。在小鼠模型实验中，在幼年小鼠中人为提高SETD7水平，即使未经历早期压力，其成年后也表现出更高焦虑和压力敏感性 1。阻断SETD7添加过量H3K4me1标记后，可防止这种DNA结构开放，使小鼠成年后行为与未受压力小鼠相似，从而保护小鼠免于成年后出现过度焦虑和压力敏感行为 1。
华盛顿大学医学院麻醉学副教授Meaghan Creed博士与普林斯顿神经科学研究所助理教授Catherine Jensen Peña博士共同担任该论文的通讯作者，其中Catherine Jensen Peña博士为资深作者 1。研究人员指出，该研究为干预早期压力导致的长期心理健康风险提供了具体生物学靶点 1。
Researchers from Washington University School of Medicine and Princeton University have discovered that early childhood stress can leave a lasting "molecular scar" in the brain, making individuals more sensitive to stress in adulthood 1. The study, conducted in St. Louis, was published in the journal Neuron on August 7, 2026 1. It reveals that early childhood stress alters the packaging of DNA in dopamine-producing neurons, thereby facilitating the activation of stress-related genes 1.
The research specifically focused on neurons in the ventral tegmental area that produce dopamine 1. Childhood stress leads to elevated levels of the enzyme SETD7, which increases the H3K4me1 chemical mark on DNA packaging 1. This epigenetic mark causes the DNA structure to become more open, allowing stress-related genes to be activated more easily 1.
To test this mechanism, researchers artificially increased SETD7 levels in young mice; even without experiencing early stress, these mice exhibited higher anxiety and stress sensitivity in adulthood 1. Conversely, blocking SETD7 from adding excess H3K4me1 marks protected the mice, resulting in adult behaviors similar to those of unstressed mice 1. Dr. Meaghan Creed, an associate professor of anesthesiology at Washington University School of Medicine, served as a co-corresponding author, while Dr. Catherine Jensen Peña, an assistant professor at the Princeton Neuroscience Institute, served as the senior and co-corresponding author of the study 1. Ultimately, this research provides a specific biological target for intervening in the long-term mental health risks caused by early-life stress 1.
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