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

基本信息

批准号：
10566856
负责人：
George Arthur Buzzell
金额：
$ 70.54万
依托单位：
FLORIDA INTERNATIONAL UNIVERSITY
依托单位国家：
美国
项目类别：
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/10566856
关键词：
15 year old Address Adolescence Adolescent Adolescent Development Affect Age Anxiety Anxiety Disorders Back Base of the Brain Behavior Biological Markers Brain Chronic Code Data Detection Development Disease Electroencephalography Ensure Evaluation Exhibits Eye 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 base bench to bedside cognitive control early adolescence frontal lobe improved male new therapeutic target novel peer predictive modeling psychologic recruit relating to nervous system response self-reported anxiety social social anxiety social cognition social interventions sociodemographics tool treatment response

项目摘要

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) 是一种慢性损害性疾病，通常出现在青春期和青少年时期。 SAD 的治疗反应率明显低于其他焦虑症。疾病，因此迫切需要确定可以为新干预措施提供信息的新治疗靶点对于这种难以治疗的疾病，我们建议通过测试一种发育信息来满足这一需求。青春期早期至中期损害性社交焦虑症状（SA）升级的机制模型；模型以对负面评价的恐惧（FNE）和在同伴面前对错误的过度警惕为中心，对额叶脑振荡的关注是这种升级的核心，青春期代表了一个敏感时期。社会认知和认知控制的发展在心理层面上表现出社会恐惧和FNE。鉴于同龄人在这一发展过程中的重要性日益增加，整个青春期的规范性有所提高在神经水平上，显示出社会认知和认知控制的额叶系统。整个青春期的长期发育，包括额叶皮层和相关 4-8 Hz 的发育 “theta”振荡与认知控制有因果关系我们的中心假设是青少年会增加。在 FNE 中，随着额叶皮层的发育，创建了一个适应不良的反馈循环：青少年变得对社交环境中的错误高度警惕，进一步增加 FNE，并最终损害我们的模型预测。（目标 1）FNE 的发展增加导致人们对存在以下情况时表现的担忧增加同行，这反过来又增强了对错误的高度警惕（即增加了与错误相关的 theta 的强度）我们进一步预测（目标 2），对错误的过度警惕会导致更加挑剔的自我。对最初恐惧的评估和确认，随着时间的推移，FNE/SA 会恶化。此外，我们预测青少年会出现这种情况。内侧额叶皮层和外侧额叶皮层的 θ 振荡表现出更大同步性的人面临的风险最大将显示 FNE/SA 的最大增幅为了测试我们的模型，我们将收集加速纵向研究。参与者包括 256 名青少年，年龄跨度为 11 至 15 岁，性别为 FNE/SA。在记录脑电图时，在同伴存在/缺席的情况下（通过 Zoom）完成修改后的认知控制任务。着眼于未来的转化工作，我们还将（目标 3）建立我们的神经测量的生态有效性考虑到升级，通过测试社交互动任务中指示 SA 的微编码行为的链接。 SA发生在青春期和更广泛的社会背景下，我们还将测量、控制和探索青春期可能的调节作用，以及社会和人口变量的影响。该提案的主要内容是我们的团队在发展精神病理学和实验方面拥有良好的记录疗法，为将该项目的发现转化为新颖的基于大脑的疗法提供了明确的途径从而缩短“从长凳到床边”的距离。