Neural pathways linking early adversity and preschool psychopathology to adolescent mental health

项目概要/摘要 学龄前焦虑，虽然普遍和损害，是一个不完美的预测未来的结果。比如说， 纵向数据表明，学龄前焦虑症不仅可以预测未来的焦虑， 内化障碍和共病的破坏性行为。同样，早期的逆境也会增加 许多青少年精神病的风险。使用我们目前的方法，我们无法确定 学龄前儿童在青春期会患上哪些疾病。这部分是因为大多数模型 主要关注诊断的连续性，而不是跨诊断风险因素，并且在 逆境，在数量上，而不是不利的童年经历的性质。目前的提案测试了 一个新的概念模型集中在不良暴露的类型上，它区分了两个主要维度 经历了多种形式的逆境：剥夺和威胁。人际暴力或威胁 认知和社会投入的减少或剥夺是根据儿童的经历类型来区分的 以及这些经历对神经和认知功能的影响。因此，这种逆境模式 允许重点关注跨诊断风险因素。重要的是，与剥夺和威胁有关的神经通路 与早期焦虑症患者的神经回路相同。考虑到这种共同的神经风险， 预期早期的逆境和焦虑会相互作用，增加青春期精神病理学的风险。我们 还期望通过其他学前诊断进一步缓和（例如，ODD、ADHD）。这些神经通路可能 是学前焦虑和青少年精神病理学之间的“缺失环节”。为了解决这个问题， 差距，我们建议以下一组青少年（现在年龄15-17岁; N=502）谁是第一次评估， 学前班（2-5岁）。这些儿童的一个子样本（N=93）进行了结构和功能成像 5-10岁之间最多3次。这一创新的、具有成本效益的提案将提供无与伦比的 有机会回答有关神经发育过程与早期风险之间关系的核心问题 青少年精神病理学的特殊形式在一个高度脆弱的人群。拟议研究 直接涉及NIMH战略计划的目标1和2。

Project Summary/Abstract Preschool anxiety, while prevalent and impairing, is an imperfect predictor of future outcomes. For example, longitudinal data suggest that anxiety disorders in preschool predict not just future anxiety but also other internalizing disorders and comorbid disruptive behavior in adolescence. Similarly, early adversity increases risk for many forms of adolescent psychopathology. Using our current methods we cannot identify which preschool children will go on to acquire which disorders in adolescence. This is in part because most models focus primarily on continuity within diagnoses as opposed to transdiagnostic risk factors and in the case of adversity, on the number rather than character of adverse childhood experiences. The current proposal tests a novel conceptual model focused on the type of adverse exposure, which differentiates two primary dimensions of experience underlying multiple forms of adversity: deprivation and threat. Interpersonal violence or threat and decreased cognitive and social inputs or deprivation are differentiated by the kind of experiences children have and by the impact of those experiences on neural and cognitive function. Thus, this model of adversity allows a focus on transdiagnostic risk factors. Importantly, the neural pathways linked to deprivation and threat are the same neural circuits known to be disrupted in early anxiety disorders. Given this shared neural risk we expect that early adversity and anxiety will interact to increase risk for psychopathology in adolescence. We also expect further moderation by other preschool diagnoses (e.g., ODD, ADHD). These neural pathways may be the ‘missing link’ between preschool anxiety and adolescent psychopathology. To address this knowledge gap, we propose following a group of adolescents (now aged 15-17 years; N=502) who were first assessed in preschool (ages 2–5 years). A subsample of these children (N=93) underwent structural and functional imaging up to 3 times between 5-10 years of age. This innovative, cost-effective proposal will provide an unparalleled opportunity to answer central questions about the trajectory of neurodevelopmental processes linking early risk to specific forms of adolescent psychopathology in a highly vulnerable population. The proposed research directly addresses Objectives 1 and 2 of the NIMH strategic plan.