Neurobiological pathways underlying maladaptive behaviors in youth

几十年的研究已经强调了弱势社区环境的破坏性影响 对以后的健康结果，包括青年反社会行为（ASB），如攻击，盗窃， 破坏公物尽管现在很少有人会质疑邻里劣势的行为后遗症， 驱动这些效应的机制尚不清楚。青少年爱滋病带菌者行为与爱滋病病毒感染的关系研究 情感和认知控制相关神经区域的功能、结构和连接 这是一个非常有希望的可能性，因为这些相同的神经过程似乎被改变， 长期的压力经历，包括不利因素。尽管可能会产生相当大的影响， 关于“生物学上的劣势嵌入”是导致ASB的一个途径的结论仍然存在 不确定，因为我们还没有确定通过哪些特定的神经机制， 邻里劣势增加青年ASB或阐明劣势如何改变这些 特定的神经通路当前的R01应用程序旨在做到这一点。我们将首先确定 与青年ASB和邻居相关的神经调节控制结构（RCA） 劣势然后，我们将利用遗传信息的性质，我们的一个一类的风险， 纵向双胞胎研究，以阐明遗传和环境的起源RCA和方式 其中，这些影响同时地和随着时间的推移被邻近不利条件改变。 对于我们的最后一组分析，我们将探索特定的邻近过程， 缺点可能影响神经RCA（即，有毒物质暴露和养育）。拟定研究 因此，理想地定位，不仅可以识别特定的神经通路， 不利因素影响青年的结果，但也要有意义地评估如何邻里 不利影响发育中的大脑。这种基于基因的发育神经科学 这种方法应该从根本上推进我们对导致神经通路的理解。 青年ASB的出现，以及邻里劣势的机制 破坏积极发展。

Decades of research have highlighted the damaging effects of disadvantaged neighborhood contexts on later health outcomes, including youth antisocial behaviors (ASB) such as assault, theft, and vandalism. Although few would now contest the behavioral sequelae of neighborhood disadvantage, the mechanism(s) driving these effects are as yet unclear. Studies linking youth ASB to alterations in the function, structure, and connectivity of affect- and cognitive control-related neural regions represent a very promising possibility, since these same neural processes appear to be altered by chronically stressful experiences including disadvantage. Although potentially quite consequential, conclusions regarding the `biological embedding of disadvantage' as a pathway to ASB remain uncertain, as we have yet to either identify the specific neural mechanisms through which neighborhood disadvantage increases youth ASB or to illuminate how disadvantage alters these particular neural pathways. The current R01 application aims to do just this. We will first identify the neural regulatory control architecture (RCA) associated with both youth ASB and neighborhood disadvantage. We will then leverage the genetically-informed nature of our one-of-a-kind at-risk, longitudinal twin study to illuminate both the genetic and environmental origins of RCA and the ways in which these influences are altered by neighborhood disadvantage, both concurrently and over time. For our final set of analyses, we will explore specific proximal processes through which neighborhood disadvantage might affect neural RCA (i.e., toxicant exposure and parenting). The proposed study is thus ideally positioned to not only identify the specific neural pathways through which neighborhood disadvantage affects youth outcomes, but also to meaningfully evaluate how neighborhood disadvantage affects the developing brain. This genetically-informed developmental neuroscience approach should fundamentally advance our understanding of both the neural pathways leading to the emergence of youth ASB, and the mechanisms through which neighborhood disadvantage undermines positive development.