Attention Training to Modify ERN and Risk for Anxiety in Adolescence

 描述（由申请人提供）：错误相关脑活动增加（由事件相关脑电位的错误相关负波（ERN）组成部分指示）被认为是焦虑的遗传风险因素。ERN和焦虑症状在怀孕期间都会急剧增加-我们的数据表明这在11岁到14岁之间尤其如此。目前的研究旨在检查ERN增加是否是焦虑增加的风险机制，以及ERN是否是斯托尼布鲁克大学和圣地亚哥州立大学招募的大型（N=600）和前瞻性青少年样本中风险的可修改生物标志物。每个研究中心将招募300名11至14岁的青少年。基于我们的试点数据，我们研究是否ERN可以改变使用自适应注意偏差修正（AABM）。AABM是一种基于计算机的方法，用于训练个人远离环境中的威胁，我们的试点数据表明AABM降低了ERN。高ERN受试者（N=300）将被随机分配至AABM组（N=150）或对照组（CC; N=150）。我们的目标是增加ERN，因为这是我们希望用AABM减少的拟议神经生物标志物。我们将研究AABM对ERN的影响，以及ERN和焦虑之间的关系，无论是在短期内（即，AABM/CC后）和2年随访时。所有参与者（即，即使是没有随机分配到AABM/CC组的低ERN参与者）也将在两年随访时返回实验室进行ERN和焦虑评估。在整个样本中，我们预测基线ERN将与焦虑相关;我们预计焦虑从基线到两年随访会增加;我们预测基线时较大的ERN将预测焦虑增加，焦虑的变化将与ERN的变化相关（目标1）。重要的是，我们预测AABM将减少ERN（目标2），ERN减少的程度将与AABM相关的焦虑减少有关（目标3）。总的来说，我们将测试 ERN是一种可改变的风险生物标志物。尽管所有随机分配到AABM组的青少年的特征是ERN相对较大，我们也将能够检查基线时较大的ERN是否能预测AABM后焦虑的变化。最后，我们进行探索性分析，以检查性别对所有假设的影响，并确定年龄是否缓和的强度，我们的主要目标，这将表明关键信息的最佳时机，以评估和修改ERN通知和影响焦虑的风险轨迹测试的关系。

 DESCRIPTION (provided by applicant): Increased error-related brain activity, as indexed by the error-related negativity (ERN) component of the event-related brain potential, has been proposed as an inherited risk factor for anxiety. Both the ERN and anxiety symptoms increase dramatically during adolescence-our data suggest this is especially true between the ages of 11 and 14. The current study aims to examine whether increased ERN is a mechanism of risk for the development of increased anxiety, and whether the ERN is a modifiable biomarker of risk among a large (N=600) and prospective sample of adolescents recruited at Stony Brook University and San Diego State University. At each site, 300 adolescents aged 11 to 14 will be recruited. Based on our pilot data, we examine whether ERN can be altered using adaptive attentional bias modification (AABM). AABM is a computer-based approach to train individuals to attend away from threat in their environments, and our pilot data suggests AABM reduces the ERN. High-ERN participants (N=300) will be randomized to AABM (N=150) or a control condition (CC; N=150). We target increased ERN precisely because this is the proposed neural biomarker we wish to reduce with AABM. We will examine the impact of AABM on ERN, and the relationship between ERN and anxiety, both in the short term (i.e., after AABM/CC) and at two year follow-up. All participants (i.e., even low-ERN participants not randomized to AABM/CC) will return to the lab to have ERN and anxiety assessed at two year follow-up. Across the entire sample, we predict that baseline ERN will relate to anxiety; we expect anxiety to increase from baseline to two year follow-up; we predict that a larger ERN at baseline will predict increased anxiety prospectively, and that changes in anxiety will relate to changes in ERN (Aim 1). Crucially, we predict that AABM will reduce the ERN (Aim 2), and that the degree to which ERN is reduced will relate to AABM-related reductions in anxiety (Aim 3). Overall, we will test whether the ERN is a modifiable biomarker of risk. Although all adolescents randomized to AABM will be characterized by a relatively large ERN, we will also be able to examine whether a larger ERN at baseline will predict change in anxiety following AABM. Finally, we conduct exploratory analyses to examine the impact of gender on all hypotheses, and determine whether age moderates the strength of the proposed relationships tested in our primary aims-which would suggest critical information about the best timing to assess and modify ERN to inform and impact anxious trajectories of risk.