Deprivation and Threat: Dimensions of Early Experience and Neural Development

剥夺和威胁：早期经历和神经发育的维度

• 批准号: 9027478
• 负责人: Katie McLaughlin
• 金额: $ 65.33万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-12-10 至 2020-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9027478
• 关键词: Address; Age; Amygdaloid structure; Animal Experimentation; Animals; Area; Biological Neural Networks; Brain; Child; Child Abuse; Childhood; Chronic; Cognitive; Data; Development; Dimensions; Disease; Early-life trauma; Emotional; Environment; Environmental Exposure; Exposure to; Extinction (Psychology); Failure; Fright; Functional Magnetic Resonance Imaging; Funding; Growth; Knowledge; Learning; Link; Measures; Mediating; Mental Health; Methods; Modeling; National Institute of Mental Health; Negative Valence; Neurophysiology - biologic function; Parietal; Parietal Lobe; Pathway interactions; Performance; Poverty; Prefrontal Cortex; Preventive Intervention; Process; Psychopathology; Research; Risk; Sampling; Severities; Specific qualifier value; Stimulus; Strategic Planning; Structure; Support System; Synapses; System; Testing; Thick; Time; Trauma; United States National Institutes of Health; abuse neglect; base; cognitive control; cohort; conditioned fear; deprivation; design; early childhood; early experience; emotion regulation; experience; neural circuit; neurodevelopment; neuroimaging; neuropsychological; novel; public health relevance; relating to nervous system; social; white matter

 DESCRIPTION (provided by applicant): Extensive research finds robust links between mental health and childhood adversity (CA), encompassing diverse exposures from child abuse to poverty. Despite the strength and consistency of these findings, the mechanisms producing such links remain poorly specified. In particular, past research has failed to identify how specifi environmental experiences influence specific neural processes. Such limitations arise from the difficulty of precisely quantifying relevant CA and neural variables in children. The current proposal addresses these limitations by capitalizing on a unique, well characterized NIH-funded longitudinal cohort of children where multiple aspects of CA have been precisely assessed and use of rigorous neuroimaging methods to quantify functioning in specific neural circuits. We will use these methods to test a novel conceptual framework delineating how specific types of environmental experience influence specific neural processes, addressing Objective 1 of the NIMH Strategic Plan. Our model argues that different types of CA have distinct effects on neural development. The central distinction we make is between trauma and deprivation. Trauma exposure involves harm or threat of harm, resulting in fear learning mediated by limbic pathways that are well characterized in animals and conserved across species. We argue that child trauma alters development of circuits in the Negative Valence System that support emotional learning encompassing amygdala and ventromedial prefrontal cortex (PFC). In contrast, deprivation involves absence of expected cognitive and social inputs and environmental complexity. Animal research shows that deprivation disrupts development in PFC and parietal cortex by hijacking the typical process of synaptic pruning. Thus we predict that social-cognitive deprivation influences Cognitive Control Systems, resulting in age-specific reductions in thickness and volume of dorsolateral PFC and superior parietal cortex and reduced performance on cognitive control tasks supported by these areas. Clearly, trauma and deprivation are correlated. Our unique design will measure these experiences on separate dimensions informed by rich preliminary data indicating distinct effects of trauma and deprivation on neural development even in samples with high exposure co-occurrence. Our proposed conceptual model will be tested by acquiring structural and functional MRI data on an existing sample of 300 children (1/3 in poverty, 1/3 near poverty, and 1/3 middle class) followed since early childhood with significant variability in CA exposure. Psychopathology has been measured in previous waves of the study and will be collected multiple times during the study period. Study findings will provide critical information about how specific dimensions of environmental experience influence specific neural processes. Elucidating these mechanisms will not only build knowledge of how adverse environments alter neural development in ways that increase risk for psychopathology, but will also suggest possible targets for preventive interventions aimed at reducing psychopathology risk in children exposed to trauma and deprivation.

 描述（由申请人提供）：广泛的研究发现心理健康和童年逆境（CA）之间存在着强有力的联系，包括从虐待儿童到贫困的各种风险。尽管这些研究结果的强度和一致性，产生这种联系的机制仍然不明确。特别是，过去的研究未能确定特定的环境经验如何影响特定的神经过程。这种局限性是由于难以精确量化儿童相关CA和神经变量。目前的提案通过利用NIH资助的独特的、特征良好的儿童纵向队列来解决这些限制，其中CA的多个方面已经得到精确评估，并使用严格的神经成像方法来量化特定神经回路的功能。我们将使用这些方法来测试一个新的概念框架，描述特定类型的环境经验如何影响特定的神经过程，解决NIMH战略计划的目标1。我们的模型认为，不同类型的CA对神经发育有不同的影响。我们所做的主要区别是创伤和剥夺。创伤暴露涉及伤害或伤害的威胁，导致由边缘系统途径介导的恐惧学习，这些途径在动物中具有很好的特征，并在物种中保守。我们认为，儿童创伤改变了负价系统的电路，支持情绪学习，包括杏仁核和腹内侧前额叶皮层（PFC）的发展。相反，剥夺涉及缺乏预期的认知和社会投入以及环境的复杂性。动物研究表明，剥夺通过劫持典型的突触修剪过程来破坏PFC和顶叶皮层的发育。因此，我们预测，社会认知剥夺影响认知控制系统，导致特定年龄的背外侧PFC和上级顶叶皮层的厚度和体积的减少，并降低这些地区支持的认知控制任务的性能。显然，创伤和剥夺是相互关联的。我们独特的设计将在不同的维度上测量这些经验，这些维度由丰富的初步数据提供信息，这些数据表明创伤和剥夺对神经发育的不同影响，即使在高暴露共现的样本中也是如此。我们提出的概念模型将通过获取现有样本的300名儿童（1/3贫困，1/3接近贫困，1/3中产阶级）的结构和功能MRI数据进行测试，这些儿童从儿童早期开始就具有显著的CA暴露变异性。在研究的前几波中已经测量了精神病理学，并将在研究期间多次收集。研究结果将提供有关环境经验的特定维度如何影响特定神经过程的关键信息。阐明这些机制不仅将建立知识的不利环境如何改变神经发育的方式，增加精神病理学的风险，但也将建议可能的目标，旨在减少儿童暴露于创伤和剥夺的精神病理学风险的预防性干预措施。