Neurodevelopmental Mechanisms Underlying Stress Vulnerability during Adolescence

青春期压力脆弱性背后的神经发育机制

• 批准号: 10599696
• 负责人: Katie McLaughlin
• 金额: $ 9.09万
• 依托单位: HARVARD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-07-01 至 2024-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10599696
• 关键词: Acceleration; Address; Adolescence; Adolescent; Age; Behavior; Child; Cognition; Cognitive; Development; Emotional; Emotions; Etiology; Exposure to; Frequencies; Grain; Individual; Institutionalization; Intervention; Knowledge; Link; Longitudinal Studies; Mental Health; Mental disorders; Methodology; Monitor; Negative Valence; Neurophysiology - biologic function; Onset of illness; Positive Valence; Process; Psychopathology; Research; Risk; Shapes; Social Behavior; Social Processes; Specificity; Stress; Stressful Event; System; Text; Time; Variant; Work; Youth; cognitive control; cohort; design; experience; innovation; longitudinal design; neglect; neural; neural circuit; novel; peer; prevent; prospective; sleep behavior; smartphone based device; social; social media; wearable device

PROJECT SUMMARY Exposure to stressful life events (SLEs) is involved in the etiology of most forms of psychopathology, and SLEs occurring early in development are particularly strong predictors of mental health problems. Most adolescent disorder onsets are temporally preceded by a major SLE. Yet, the mechanisms linking SLEs to the onset of adolescent psychopathology remain poorly understood. Prior research on mechanisms linking SLEs with youth mental disorders has focused largely on severe forms of adversity like abuse, neglect, and institutionalization. It is unknown whether similar mechanisms are involved in the link between less severe SLEs and psychopathology. Perhaps more critically, existing work has relied largely on cross-sectional between-subjects designs that compare children with exposure to some type of SLE to children without that experience. There is a dearth of longitudinal studies examining how SLEs influence emotion, cognition, behavior, and neural circuits within-individuals over time in ways that predict the emergence of psychopathology. The proposed research addresses this gap, using a novel methodological approach that permits examination of dynamic changes in emotion, cognition, social behavior, and neural function and connectivity following SLEs at a sufficiently fine grained level of temporal specificity to identify mechanisms underlying the link between SLEs and adolescent psychopathology as they unfold in real time. Specifically, the project will examine how monthly fluctuations in exposure to SLEs within-individuals predict subsequent changes in emotional processing in the Negative and Positive Valence Systems, Cognitive Control, Social Processes, and neural function and connectivity over a 12-month period. In addition to monthly assessments of SLEs, psychopathology, and potential mechanisms, passive monitoring of activity, sleep, and social behavior (e.g., interaction with peers through text and social media) through smartphones and wearable devices will allow additional mechanisms to be assessed passively and without subject burden. The study will investigate whether monthly variation in these emotional, cognitive, social, and neural processes predicts later increases in internalizing and externalizing problems in an accelerated cohort design with monthly assessments spanning age 11-18 years, producing 1,680 monthly observations over the study period. The longitudinal design and high-frequency assessments are innovative in allowing the identification of mechanisms that are altered by SLEs and prospectively predict psychopathology with high temporal specificity during a developmental period associated with increases in SLE exposure, stress vulnerability, and risk for psychopathology. Study findings will provide critical information regarding the specific domains of emotion, cognition, social behavior, and neural function that are altered by exposure to SLEs and increase vulnerability to psychopathology. These mechanisms represent modifiable targets for interventions to prevent the onset of stress-related psychopathology in children and adolescents.

项目概要 暴露于压力性生活事件 (SLE) 是大多数精神病理学形式的病因，而 SLE 发生在发育早期是心理健康问题的特别有力的预测因素。大多数青少年 严重系统性红斑狼疮暂时先于疾病发作。然而，系统性红斑狼疮 (SLE) 与疾病发作之间的联系机制 青少年精神病理学仍然知之甚少。先前关于系统性红斑狼疮与青少年联系机制的研究 精神障碍主要集中于严重的逆境，如虐待、忽视和收容。 目前尚不清楚不太严重的 SLE 和较轻的 SLE 之间的联系是否涉及类似的机制。 精神病理学。也许更关键的是，现有的工作很大程度上依赖于跨学科的跨学科研究 设计将接触过某种类型 SLE 的儿童与没有这种经历的儿童进行比较。有 缺乏研究系统性红斑狼疮如何影响情绪、认知、行为和神经回路的纵向研究 随着时间的推移，个体内部的变化可以预测精神病理学的出现。拟议的研究 通过使用一种新颖的方法来解决这一差距，该方法允许检查动态变化 SLE 后的情绪、认知、社会行为、神经功能和连接性在足够精细的情况下 时间特异性的粒度水平，以确定系统性红斑狼疮和青少年之间联系的潜在机制 实时展开的精神病理学。具体来说，该项目将研究每月的波动情况 个体暴露于系统性红斑狼疮可预测消极和消极情绪处理的后续变化 正价系统、认知控制、社会过程以及神经功能和连接 12个月期限。除了每月评估系统性红斑狼疮、精神病理学和潜在机制外， 被动监测活动、睡眠和社交行为（例如，通过文本和社交媒体与同伴互动） 媒体）通过智能手机和可穿戴设备将允许被动评估额外的机制 并且没有主题负担。该研究将调查这些情绪、认知、 社会和神经过程预测随后的内化和外化问题的增加 加速队列设计，每月进行 11-18 岁评估，每月产生 1,680 份 研究期间的观察结果。纵向设计和高频评估具有创新性 允许识别 SLE 改变的机制并进行前瞻性预测 在发育时期具有高度时间特异性的精神病理学，与增加 SLE 暴露、压力脆弱性和精神病理学风险。研究结果将提供关键信息 关于情绪、认知、社会行为和神经功能的特定领域 接触系统性红斑狼疮并增加患精神病理学的可能性。这些机制代表可修改的 预防儿童和青少年发生与压力相关的精神病理学的干预措施目标。