Neurophysiological and Metabolic Risk Markers of Childhood Anxiety

项目摘要/摘要 焦虑症是儿童时期最常见的精神疾病，影响着10%-20%的年轻人。 儿童焦虑通常有一个慢性病程，对学习、社交和适应能力产生负面影响。 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，这些因素 可能有助于焦虑的发展和维持。然而，人们对此的了解有限。 焦虑的最早先兆或多种风险因素如何在发育内部和整个发展过程中相互影响 焦虑风险。需要从婴儿期开始的前瞻性研究来解释焦虑的起源，以便(A) 可以发现在出现症状和(B)之前识别高危儿童的生物标记物 可以针对高危儿童制定和实施预防战略。当前的总体目标是 该项目旨在测试神经、生理、行为和环境风险因素在 早年的生活容易受到童年焦虑的影响。这项研究的目标将通过遵循既定的 纵向队列(R01 MH078829；N=807)。目前的研究将建立在一个广泛的数据库的基础上 包括神经生理学(脑电、事件相关电位)、神经代谢功能(FNIRS)、 生理应激反应、对威胁反应的行为指标和家庭环境风险 (母亲精神病理学，压力暴露)，从婴儿期到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。在这些年龄段，我们将对我们的队列进行表型 焦虑症状学，以及实施一系列基于大脑的措施，类似于在 年龄3岁。分析将测试早期神经处理模式(在婴儿期和3岁时再次出现 年)预测日后焦虑的风险；检查神经、生理、行为和家庭的测量 环境因素共同促进焦虑的发展；并探索不同的焦虑模式 危险因素和发展轨迹预测不同的焦虑表型。我们预计调查结果 将(A)阐明焦虑症的神经发育基础，(B)有助于发现非侵袭性 可识别高危儿童的生物标志物，以及(C)为设计创新战略提供信息，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.