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 睡眠越来越被认为是大脑健康和发育的关键因素。 睡眠问题存在于超过90%的焦虑青年中，预测恶化 症状，并且在治疗相关的焦虑缓解后不消退， 处于持续风险中的青少年（综述参见McMakin等人，2015年）的报告。然而，我们几乎没有可测试的模型， 睡眠相关问题究竟如何以及为什么会影响年轻人的心理健康， 很难理解风险病理学并进行精确干预。睡眠和焦虑 不同发展阶段之间的差异很大，使情况进一步复杂化。 从睡眠对认知和情感功能的已知作用中得出的模型（例如， 记忆巩固，情绪调节）来解释这些过程中的中断如何能够 在敏感的发展时期，需要驱动特定的症状， 性新为此，我们正在进行的R 01旨在测试我们的理论模型， 睡眠神经生理学的关键特征（例如，宏观觉醒、纺锤体活动）影响情绪 反应性和记忆处理，以驱动消极的过度概括（目标1和2）。我们也 检查这种依赖睡眠的过程是否可以修改（目标3）。尽管方法论 复杂性和全球流行病，我们即将完成目标1的数据收集工作， 2（96%; n=192/200），结果支持我们模型的关键特征。所述补充剂被 要求支持目标3的关键完成（n=60），其中我们将注意力转向 改变这些过程的潜力。具体来说，我们将使用定向记忆激活 在睡眠期间操纵哪些记忆被选择用于巩固。如果我们能成功地 修改记忆选择，这导致睡眠微结构的变化与睡眠微结构的变化相一致。 减少消极的过度概括，我们不仅会在我们的理论中获得对因果关系的支持， 此外，我们也将为干预工作做好准备。