Sleep-dependent negative overgeneralization in peri-pubertal anxiety

围青春期焦虑中睡眠依赖性消极过度概括

• 批准号: 10733895
• 负责人: DANA L MCMAKIN
• 金额: $ 8.35万
• 依托单位: FLORIDA INTERNATIONAL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-06-01 至 2024-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10733895
• 关键词: Affect; Affective; Anxiety; Arousal; Attention; Cognitive; Data; Data Collection; Development; Dimensions; Disease remission; Emotional; Etiology; Functional disorder; Funding; Health; Intervention; Lead; Memory; Mental Health; Methodology; Modeling; Pathology; Pattern; Persons; Positioning Attribute; Process; Puberty; Risk; Role; Sleep; Structure; Symptoms; Testing; Theoretical model; Work; Youth; anxiety symptoms; brain health; emotion regulation; improved; memory consolidation; memory process; neuromechanism; neurophysiology; pandemic disease

PROJECT SUMMARY Sleep is increasingly understood as a critical contributor to brain health and development. Problems with sleep are present in more than 90% of youth with anxiety, predict worsening symptoms, and do not resolve following treatment-related remission of anxiety, leaving these youth at ongoing risk (for review see McMakin et al., 2015). Yet, we have few testable models for exactly how and why sleep-related problems impact mental health in young people, making it hard to understand risk pathology and intervene with precision. Both sleep and anxiety are heterogeneous and vary significantly across development, further complicating the picture. Models that draw from the known roles of sleep for cognitive and affective functions (e.g., memory consolidation, emotion regulation) to explain how disruptions in these processes could drive specific symptoms during sensitive periods of development are needed to move the field forward. To this end, our ongoing R01 aims to test our theoretical model whereby disruptions in key features of sleep neurophysiology (e.g., macro-arousals, spindle activity) impact emotional reactivity and memory processing to drive negative overgeneralization (Aims 1 and 2). We also examine whether this sleep-dependent process is modifiable (Aim 3). Despite methodological complexity and a global pandemic, we are nearing completion of data collection for Aims 1 and 2 (96%; n=192/200) with results supporting key features of our model. The supplement is requested to support the critical completion of Aim 3 (n=60) in which we turn our attention to the potential to modify these processes. Specifically, we will use targeted memory reactivation during sleep to manipulate which memories are selected for consolidation. If we can successfully modify memory selection and this leads to changes in sleep microstructure coincident with a reduction in negative overgeneralization, we will not only gain support for causality within our model but also, we will be well-positioned for intervention work.

项目摘要 睡眠越来越被理解为造成大脑健康和发育的关键因素。 超过90％的焦虑症患者存在睡眠问题，预测恶化 症状，并且在与治疗相关的焦虑缓解后无法解决，而这些 持续风险的青年（有关审查，请参见McMakin等，2015）。但是，我们几乎没有可测试的模型 确切的方式以及为什么与睡眠有关的问题影响年轻人的心理健康， 很难理解风险病理并精确干预。睡眠和焦虑都是 在整个开发中，异质性和变化显着，使情况变得更加复杂。 从已知的睡眠作用中汲取认知和情感功能的模型（例如， 记忆合并，情绪调节）解释这些过程中的破坏如何 需要在敏感的开发期间驱动特定症状才能移动现场 向前。为此，我们正在进行的R01旨在测试我们的理论模型，从而破坏 睡眠神经生理学的关键特征（例如，宏观主体，主轴活动）影响情绪 反应性和记忆加工以驱动负面概括（目标1和2）。我们也是 检查这种与睡眠有关的过程是否可修改（AIM 3）。尽管有方法论 复杂性和全球大流行，我们接近完成目标1和 2（96％; n = 192/200），结果支持我们模型的关键特征。补充是 要求支持AIM 3（n = 60）的关键完成，我们将注意力转移到 修改这些过程的潜力。具体来说，我们将使用目标内存重新激活 在睡眠过程中，以操纵选择哪些记忆进行整合。如果我们能成功 修改内存选择，这导致睡眠微观结构的变化与 减少负面概括过度，我们不仅会在我们的因果关系中获得支持 但是，我们还将有充分的态度进行干预工作。