Neurobiological characteristics, parent-child relationships, and conduct problems in adolescence: A longitudinal multimodal neuroimaging study

项目摘要 儿童和青少年的行为问题，包括攻击性和违反规则的行为 是未来犯罪行为的重要风险因素。一种可能的机制涉及非典型发育 高危个体的大脑结构和/或功能与奖惩处理有关。 降低的奖励敏感度可能会通过尝试“正常化”来驱动不适应的奖励寻求行为 与奖赏相关的神经反应，并可能导致适当行为的学习受损。论 另一方面，惩罚敏感性的减弱可能会增加反社会行为的风险，因为 没有在线索和负面结果之间建立联系的个体没有焦虑和 每当考虑从事反社会行为时，都会产生预期的恐惧。然而，之前的大部分 研究是跨领域的。本研究的目的是了解行为的起源和发展 从纵向角度看问题，通过反复评估风险因素(报酬减损/ 惩罚处理)从童年到青春期，识别脆弱的神经底物 支持这些过程，并确定环境因素的调节效果(即，父母- 子女关系)。 利用神经行为测量在8-9岁时被客观评估的现有队列 (SC2HD076044，PI：GAO)，目前的项目提议重新评估 参与者每年从14-15岁开始，为期三年。我们将评估生物和社会风险因素 使用与先前研究中使用的电池相同的电池(经过适合年龄的修改)，以及年龄- 适当的心理社会风险因素和行为结果评估。此外，我将在我的基础上 目前的SC3资助(SC3GM118233，PI：GAO)并利用纵向多模式磁共振 磁共振成像方法研究奖惩相关回路功能的变化 处理(使用功能磁共振成像)和白质连接(使用扩散张量成像)跨越1.5年 来自同一群人的时期。我的中心假设是奖惩的非典型发展 从童年到青春期的过程将与更多的行为问题相关，而且这是积极的 亲子关系将缓冲神经脆弱性对行为问题发展的影响。 该项目的完成将推进美国国立卫生研究院大脑计划的使命，即了解电路和 产生心理体验和行为的神经活动模式“。了解神经和 有助于与行为问题相关的奖惩处理的自主机制具有 揭示参与这些疾病发展的潜在的精神病理过程的可能性 并将改进病因学模型，为干预和治疗提供基础。

Project Abstract Conduct problems, which include aggression and rule-breaking behavior, in children and adolescence are significant risk factors for future criminal behavior. One possible mechanism involves atypical development of brain structure and/or function implicated in reward and punishment processing in at-risk individuals. Reduced reward sensitivity may drive maladaptive reward seeking behavior via attempts to “normalize” reward-related neural reactivity, and may result in compromised learning of appropriate behaviors. On the other hand, weakened punishment sensitivity may increase the risk of antisocial behavior because the individual failing to form associations between cues and negative consequence does not have anxiety and anticipatory fear whenever contemplating the engagement in an antisocial act. However, most of the prior research is cross-sectional. The objective of this study is to understand the origin and development of conduct problems from a longitudinal perspective, by repeatedly assessing the risk factors (impaired reward/ punishment processing) from childhood to adolescence, identifying the vulnerable neural substrates underpinning these processes, and determining the modulating effects of environmental factors (i.e., parent- child relationship). Capitalizing on an existing cohort whose neurobehavioral measures were objectively assessed at 8-9 years and again at 9-10 years (SC2HD076044, PI: Gao), the current project proposes to re-assess the participants annually starting at 14-15 years for three years. We will assess biological and social risk factors using a battery identical (with age-appropriate modifications) to the one used in prior studies, as well as age- appropriate psychosocial risk factor and behavioral outcome assessments. Moreover, I will build upon my current SC3 funding (SC3GM118233, PI: Gao) and utilize a longitudinal multi-modal Magnetic Resonance Imaging (MRI) approach to study the changes in function of the circuitry implicated in reward/punishment processing (using fMRI) and the white-matter connections (using Diffusion Tensor Imaging) across a 1.5-year period from the same cohort. My central hypotheses are that atypical development of reward/punishment processing from childhood to adolescence will be associated with more conduct problems, and that positive parent-child relationship will buffer the effect of neural vulnerability on the development of behavioral problems. Completion of this project will advance the mission of the NIH BRAIN Initiative to “understand the circuits and patterns of neural activity that give rise to mental experience and behavior”. Understanding the neural and autonomic mechanisms that contribute to the reward/punishment processing related to conduct problems has the potential to uncover underlying psychopathological processes involved in the development of these problems, and will improve etiological models that provide the foundation for intervention and treatment.