A developmentally-sensitive mechanism underlying the escalation of adolescent social anxiety

青少年社交焦虑升级的发育敏感机制

• 批准号: 10707188
• 负责人: George Arthur Buzzell
• 金额: $ 68.66万
• 依托单位: FLORIDA INTERNATIONAL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-09-20 至 2027-06-30
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10707188
• 关键词: 15 year old; Acceleration; Address; Adolescence; Adolescent; Adolescent Development; Affect; Age; Anxiety; Anxiety Disorders; Back; Behavior; Biological Markers; Brain; Chronic; Code; Data; Detection; Development; Disease; Electroencephalography; Ensure; Evaluation; Exhibits; Feedback; Feeds; Female; Female Adolescents; Fright; Future; Goals; Impairment; Intervention; Investigational Therapies; Lateral; Lead; Link; Longitudinal Studies; Measures; Medial; Mediating; Methods; Modeling; National Institute of Mental Health; Neurocognitive; Participant; Pathway interactions; Patient Self-Report; Performance; Play; Population; Positioning Attribute; Prevention; Psychopathology; Puberty; Risk; Role; Self-Examination; Social Anxiety Disorder; Social Development; Social Environment; Social Interaction; System; Testing; Theoretical model; Therapeutic; Time; Translating; Work; anxiety symptoms; anxious behavior; bench to bedside; brain based; cognitive control; early adolescence; frontal lobe; improved; male; neural; new therapeutic target; novel; peer; predictive modeling; psychologic; recruit; response; self-reported anxiety; social; social anxiety; social cognition; social interventions; sociodemographics; tool; treatment response

Abstract Social anxiety disorder (SAD) is a chronic, impairing condition that typically emerges during adolescence and affects about 10% of the population. Treatment response rates for SAD are markedly lower than for other anxiety disorders, thus presenting an urgent need to identify novel therapeutic targets that can inform new interventions for this difficult-to-treat disorder. We propose to address this need by testing a developmentally-informed, mechanistic model of the escalation of impairing social anxiety symptoms (SA) in early-to-mid adolescence; our model centers on Fear of Negative Evaluation (FNE) and Hypervigilance for Errors in the presence of peers, with a focus on frontal brain oscillations as central to this escalation. Adolescence represents a sensitive period for the development of social cognition and cognitive control. At the psychological level, social fears and FNE exhibit normative increases across adolescence, given the increasing importance of peers during this developmental window. At the neural level, frontal brain systems underlying social cognition and cognitive control exhibit protracted development across adolescence, including development of the frontal cortex and associated 4-8 Hz “theta” oscillations causally implicated in cognitive control. Our central hypothesis is that adolescent increases in FNE, alongside development of the frontal cortex, create a maladaptive feedback loop: adolescents become Hypervigilant to Errors in social settings, further increasing FNE, and ultimately, impairing SA. Our model predicts (Aim 1) that developmental increases in FNE lead to increased concerns over performance in the presence of peers, which in turn amplifies Hypervigilance for Errors (that is, increased strength of error-related theta oscillations). We further predict (Aim 2) that increased Hypervigilance for Errors leads to more critical self- evaluations and confirmations of initial fears, which worsen FNE/SA over time. Moreover, we predict adolescents who exhibit greater synchrony in theta oscillations across medial-lateral frontal cortex are at greatest risk and will display the largest increases in FNE/SA. To test our model, we will collect an accelerated longitudinal study of 256 adolescents, spanning ages 11-15, biologically male/female, and ranging in FNE/SA. Participants will complete a modified cognitive control task in peer presence/absence (via Zoom) as EEG is recorded. With an eye toward future translational work, we will also (Aim 3) establish the ecological validity of our neural measures by testing links to micro-coded behaviors indicative of SA within a social interaction task. Given that escalation of SA occurs during puberty and within a broader social context, we will also measure, control for, and explore the possible moderating roles of puberty, as well as effects of social and demographic variables. A key strength of this proposal is that our team has a proven record in developmental psychopathology and experimental therapeutics, providing a clear path for translating findings from this project into novel, brain-based therapeutics and thereby shortening the distance “from bench to bedside.”

抽象的 社交焦虑症（SAD）是一种慢性，损害的疾病，通常在青少年和 影响约10％的人口。 SAD的治疗反应率明显低于其他焦虑 疾病，因此迫切需要确定可以告知新干预措施的新型治疗靶标 对于这种难以治疗的疾病。我们建议通过测试已发达的， 在早期至中间的社交焦虑症状（SA）升级的机理模型；我们的 模型以担心负面评估（FNE）和对同行存在的错误的过度维护为中心 重点是额叶脑振荡，这是这一升级的核心。青少年代表一个敏感的时期 社会认知和认知控制的发展。在心理层面，社会恐惧和FNE展览 鉴于这种发展期间同龄人的重要性越来越高，青少年的正常增加 窗户。在神经层面，社会认知和认知控制退出的基础额脑系统 跨青春期的发育发育，包括额叶皮层的发展和相关的4-8 Hz “ theta”振荡与认知控制有关。我们的中心假设是青少年增加 在FNE，除了额叶皮层的开发外，创建一个不良适应反馈循环：青少年成为 对社会环境中的错误有利，进一步增加了FNE，最终会损害SA。我们的模型预测 （AIM 1）FNE的发展增加导致人们对在存在的情况下的性能提高 同龄人，这又是放大器过度维护误差（即，与错误相关的theta的强度提高 振荡）。我们进一步预测（AIM 2），增加了错误的过度维护，从而导致更关键的自我 对最初恐惧的评估和确认，这会随着时间的流逝而恶化。此外，我们预测青少年 在媒体上外侧皮层跨theta振荡中暴露了更大的同步的人，风险最大， 将显示FNE/SA的最大增加。为了测试我们的模型，我们将收集一项加速的纵向研究 256名青少年，跨越11-15岁，男性/女性，范围为fne/sa。参与者会 在记录脑电图时（通过缩放）在同伴存在/不存在（通过变焦）中完成修改的认知控制任务。与 着眼于未来的翻译工作，我们还将（AIM 3）建立神经测量的生态有效性 通过测试指示社会互动任务中SA的微编码行为的链接。鉴于这种升级 SA发生在青春期期间，在更广泛的社会环境中，我们还将衡量，控制和探索 青春期的可能调节作用以及社会和人口变量的影响。关键力量 该提议的是，我们的团队在发育心理病理学和实验性方面具有可靠的记录 疗法，为将该项目的发现转化为基于大脑的新型疗法提供了清晰的途径 从而缩短了“从长凳到床边”的距离。