A Neuroecological Approach to Examining the Effects of Early Life Adversity on Adolescent Drug Use Vulnerabilities Using the ABCD Dataset

项目摘要 早期生活逆境(ELA)是神经认知风险的一个多维和潜在的风险因素，下游 毒品使用脆弱性以及青少年吸毒和滥用。ELA对青少年吸毒风险的影响 依赖于多种动态的家庭、同龄人、学校、社区和社会文化风险和保护环境。 然而，缺乏一个重要的知识基础来加深我们对神经细胞 生物标志物影响青春期的药物风险、脆弱性和行为。 新兴的研究和理论表明，神经调节系统是情绪和行为的基础 监管是青少年药物使用风险调查的有力重点。我们关注的是个体差异 神经调节系统，认知控制网络随着时间的推移在调节方面变得更加有效 情绪处理网络，包括情绪/显著网络和奖励显著网络。根据这一点 双重系统观点，社会情绪网络(或ERSN)之间的神经调节失衡，由 情绪、奖励和显著网络)和CCN导致自我调节能力减弱 青春期的毒品危险行为是其基础。这种发育机制和随后的危险行为 可能受到青年维度压力的不同影响。现有的发育研究已经编目了 缓和ELA的影响和药物使用发展的心理社会风险和保护过程 青春期的脆弱性。然而，在神经科学的方法中，生态方法仍然很少见。使用 发展生态神经科学方法，我们建议研究神经认知机制， 调节ELA对药物相关脆弱性和药物的影响的背景因素 使用。我们将重点研究ELA对功能激活和沟通的发育变化的影响 (即，功能连接；FC)ERSN和CCN网络之间及其在导致 青少年药物使用脆弱性和后来的药物使用。 我们建议使用一个大型的纵向数据集：青少年大脑认知发展研究 (ABCD；N=11,883；基线年龄9-10岁，第6波年龄11.5-12.5岁)。我们的目标是测试(A)发育 ELA对药物使用易感性和伴随药物使用的影响的认知机制 误用(B)家庭、同伴、学校、社区和社会文化背景对 导致药物使用脆弱性的神经认知过程。模拟多层次的生态潜伏变化， 行为和神经成像数据对于进一步研究发育模型的精确度和特异性至关重要 以及青春期药物成瘾复原力的预防性干预计划。

Project Summary Early life adversity (ELA) is a multidimensional and potent risk factor for neurocognitive risk, downstream drug use vulnerabilities, and adolescent drug use and misuse. The effects of ELA on youth’s drug use risk depend on multiple dynamic family, peer, school, community, and sociocultural risk and protective contexts. Yet, a significant knowledge base is missing to further our understanding of the contexts in which neural biomarkers affect drug risk vulnerabilities and behaviors in adolescence. Emerging research and theory implicate neuroregulatory systems that underpin emotion and behavioral regulation as a powerful focus for adolescent drug use risk investigations. We focus on individual differences in neuroregulatory systems whereby cognitive control networks become more effective over time in modulating emotion processing networks, including the emotion/salience and reward salience networks. According to this dual system view, a neuroregulatory imbalance between the socioemotional network (or ERSN, comprised of the emotional, reward, and salience networks) and CCN ushers in diminished self-regulation abilities that underlie drug risk behaviors in adolescence. This developmental mechanism and subsequent risk behaviors may be differentially affected by youth’s dimensional stress. Extant developmental studies have cataloged psychosocial risk and protective processes that moderate the impact of ELA and the development of drug use vulnerabilities in adolescence. Yet ecological approaches remain rare in neuroscience approaches. Using a developmental ecological neuroscience approach, we propose to investigate neurocognitive mechanisms that mediate, and the contextual factors that moderate, the effect of ELA on drug-related vulnerabilities and drug use. We will focus on the impact of ELA on developmental changes in functional activation and communication (i.e., functional connectivity; FC) between the ERSN and CCN networks and its mechanistic role in leading to adolescent drug use vulnerabilities and later drug use. We propose to use a large, longitudinal dataset: the Adolescent Brain Cognitive Development Study (ABCD; N=11,883; ages 9-10 at baseline and 11.5-12.5 at wave 6). We aim to test (a) the developmental cognitive mechanisms that mediate the effect of ELA on drug use vulnerabilities and attendant drug use and misuse (b) the moderating influence of family, peer, school, community, and sociocultural contexts on the neurocognitive processes that lead to drug use vulnerabilities. Modeling multilevel latent change in ecological, behavioral, and neuroimaging data is critical to further the precision and specificity of developmental models and preventative intervention programs for drug addiction resilience in adolescence.