Neurophysiological and Metabolic Risk Markers of Childhood Anxiety

项目总结/摘要 焦虑症是儿童期最常见的精神疾病，影响10-20%的青少年。 儿童期焦虑通常具有慢性过程，对学业、社会和适应功能产生负面影响， 并增加了一生中患精神疾病的风险。研究强调了一些风险因素， 可能会导致焦虑的发展和维持。然而，人们对这一问题的认识有限。 焦虑的最早前兆或多种风险因素如何在发展过程中相互作用， 焦虑风险从婴儿期开始的前瞻性研究需要解释焦虑的起源，以便（a） 可以发现在症状出现之前识别处于风险中的儿童的生物标志物，以及（B） 可以为有风险的儿童制定和实施预防战略。当前的总体目标 项目是测试神经，生理，行为和环境风险因素的综合影响， 早期生活对童年焦虑的脆弱性。研究目标将通过以下既定的 纵向队列（R 01 MH 078829; N=807）。目前的研究将建立在一个广泛的数据库基础上， 包括神经生理学（EEG，ERP），神经代谢功能（fNIRS）， 生理应激反应、对威胁的行为反应指标和家庭环境风险 （母亲的精神病理学，压力暴露）之间的婴儿期和年龄3岁。在目前的提案中，我们 寻求资金支持5岁和7岁的后续研究。在这些年龄，我们将表型我们的队列， 焦虑情绪学，以及实施一系列基于大脑的措施，类似于在 年龄3岁。分析将测试早期的神经处理模式（婴儿期和3岁时）是否 年）预测以后焦虑的风险;检查神经，生理，行为和家庭的措施 环境因素共同促进焦虑的发展;并探讨不同的模式是否 风险因素和发展轨迹预测不同的焦虑表型。我们希望调查结果 将（a）阐明焦虑的神经发育基础，（B）有助于发现非侵入性的 生物标志物，可以识别处于危险之中的儿童和（c）告知创新战略的设计，以防止 焦虑的发展。

PROJECT SUMMARY/ABSTRACT Anxiety disorders are the most common psychiatric illnesses of childhood, affecting 10-20% of youth. Childhood anxiety often has a chronic course, negatively affecting academic, social, and adaptive functioning, and increases the risk for mental illness throughout life. Research has highlighted a number of risk factors that likely contribute to the development and maintenance of anxiety. However, there is limited understanding of the earliest precursors of anxiety or how multiple risk factors interact within and across development to influence anxiety risk. Prospective studies beginning in infancy are needed to explicate the origins of anxiety so that (a) biomarkers can be discovered that identify at-risk children prior to the emergence of symptoms and (b) preventive strategies can be developed and implemented with at-risk children. The overall goal of the current project is to test the combined effects of neural, physiological, behavioral, and environmental risk factors in early life on vulnerability to childhood anxiety. The study aims will be accomplished by following an established longitudinal cohort (R01 MH078829; N=807). The current study will build on an extensive database that includes repeated assessments of neurophysiology (EEG, ERP), neural metabolic functioning (fNIRS), physiological stress reactivity, behavioral indicators of reactivity to threat, and family environmental risk (maternal psychopathology, stress exposures) between infancy and age 3 years. In the current proposal, we seek funds to support a follow up study at ages 5 and 7 years. At these ages, we will phenotype our cohort for anxiety symptomatology, as well as implement a battery of brain-based measures similar to what was used at age 3 years. Analyses will test whether early patterns of neural processing (in infancy and again at age 3 years) predict risk for later anxiety; examine how measures of neural, physiological, behavioral, and family environment factors jointly contribute to the development of anxiety; and explore whether different patterns of risk factors and trajectories of development predict different anxiety phenotypes. We expect that the findings will (a) elucidate the neurodevelopmental bases of anxiety, (b) contribute to the discovery of non-invasive biomarkers that can identify at-risk children and (c) inform the design of innovative strategies to prevent the development of anxiety.