Independent and interactive effects of genetic risk for depression and family income-to-needs on emotional brain development and behavior

抑郁症遗传风险和家庭收入需求对情绪脑发育和行为的独立和交互影响

• 批准号: 10678577
• 负责人: Claire Edwards Campbell
• 金额: $ 4.77万
• 依托单位: UNIVERSITY OF SOUTHERN CALIFORNIA
• 依托单位国家: 美国
• 财政年份: 2023
• 资助国家: 美国
• 起止时间: 2023-05-16 至 2025-05-15
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10678577
• 关键词: 10 year old; 12 year old; Address; Adolescence; Adolescent; Adult; Affect; Age; Age Years; Amygdaloid structure; Area; Behavior; Behavioral; Biological Markers; Brain; Brain imaging; Child; Childhood; Classification; Cognitive; Communities; Complex; Data; Development; Disease; Early Diagnosis; Early Intervention; Early treatment; Emotional; Environment; Environmental Exposure; Environmental Risk Factor; Family; Foundations; Functional Magnetic Resonance Imaging; Genes; Genetic; Genetic Risk; Goals; Grant; Health; Hippocampus; Household; Income; Individual; Individual Differences; Influentials; Investigation; Life; Long-Term Effects; Low income; MRI Scans; Maps; Measures; Mediating; Mental Depression; Mental disorders; Methodology; Modeling; Onset of illness; Outcome; Persons; Policy Maker; Population; Poverty; Publishing; Recurrence; Research; Research Personnel; Rest; Risk; Risk Factors; Sampling; Scientist; Severities; Shapes; Site; Socioeconomic Status; Structure; Surface; Symptoms; Testing; Thick; Time; Training; United States; Withdrawal Symptom; Work; World Health Organization; Youth; behavioral outcome; brain behavior; brain circuitry; brain size; burden of illness; child depression; cognitive control; cognitive development; depressive symptoms; early adolescence; early detection biomarkers; early onset; emotional behavior; federal poverty level; follow-up; gene environment interaction; improved; intervention program; morphometry; neural; neurodevelopment; neuroimaging; polygenic risk score; recurrent depression; single episode major depressive disorder; skills; social health determinants; treatment program; young adult

PROJECT SUMMARY / ABSTRACT Depression is one of the major contributors to the global burden of disease, with the World Health Organization (WHO) ranking it as the number one non-fatal contributor. Most cases of depression appear by an individual’s third decade of life, which is classified as early onset depression. The long-term effects of early onset depression extend well into adulthood, usually leading to a high rate of recurrence and significant health concerns. Research has shown that early intervention prior to disease onset leads to the best outcomes. Therefore, detecting early markers of depression risk would help mitigate the disease. Previous investigations have looked at the effect of environmental exposures or genetic influences separately, with studies beginning to examine the interactive effects of genes and the environment on risk for depression. Though, few studies have been done examining how gene-by-environment interactions may map onto prodromal brain and behavioral biomarkers of risk for early onset depression, which could greatly assist in early detection and treatment. Specifically, select brain structure and functional networks as well as distinct emotional behaviors – such as, positive affect and withdrawal symptoms – have been consistently associated with early onset depression. Ultimately, it suggests that these may be important biomarkers in studying how gene-by-environment may contribute to risk for depression that emerges prior to disease onset. Thus, this study will examine whether the well-known environmental predictor of family income-to-needs may have independent and/or interactive effects along with an individual’s polygenic risk score for depression on the development of emotional brain structure and function from pre- to early adolescence. To accomplish this goal, the current study will leverage existing longitudinal data from approximately 5,000 subjects 9-10 year-of-age at baseline to 11-12 year-of-age at the 2-year follow-up from across the United States as part of the larger Adolescent Brain Cognitive Development? Study (ABCD Study®). Using two time point data for the brain imaging and up to three time points for emotional behavior outcome data, we will examine how gene-by-environment interactions effect changes in brain size and function. Aim 1 and Aim 2 will examine the independent and interactive effect of an individual’s income-to-needs and polygenic risk for depression on functional brain connectivity and brain structure of key emotional regions previously associated with depression, respectively. Aim 3 will further test whether the income-to-needs and polygenic risk score relate to established prodromal emotional behaviors. Ultimately, the findings from this project hold the potential to identify potential brain-behavior biomarkers that may be important to consider in establishing risk for early onset depression, ultimately helping to improve early detection and treatment.

项目概要/摘要 世界卫生组织认为，抑郁症是造成全球疾病负担的主要原因之一 （世界卫生组织）将其列为第一大非致命因素，大多数抑郁症病例都是由个人的原因引起的。 生命的第三个十年，被归类为早发性抑郁症 早发性抑郁症的长期影响。 持续到成年期，通常会导致高复发率和严重的健康问题。 已经表明，在疾病发作之前进行早期干预可以带来最佳结果。 抑郁症风险的标志物将有助于减轻这种疾病的影响。 环境暴露或遗传影响分别，研究开始检验交互作用 然而，很少有研究探讨基因和环境对抑郁症风险的影响。 基因与环境的相互作用如何映射到前驱期大脑和早期风险的行为生物标志物 发病抑郁症，这可以极大地帮助早期发现和治疗，具体来说，选择大脑结构。 和功能网络以及独特的情绪行为——例如积极的情感和退缩 症状——一直与早发性抑郁症相关。最终，这表明这些症状。 可能是研究基因与环境如何导致抑郁症风险的重要生物标志物 因此，本研究将检验众所周知的环境预测因素是否存在。 家庭收入与需求的关系可能与个人的多基因一起产生独立和/或相互作用的影响 抑郁症风险评分对情绪脑结构和功能从学前到早期发育的影响 为了实现这一目标，当前的研究将利用现有的纵向数据。 大约 5,000 名基线时年龄为 9-10 岁的受试者到 2 年随访时年龄为 11-12 岁的受试者 作为更大规模的青少年大脑认知发展研究 (ABCD Study®) 的一部分？ 使用两个时间点数据进行大脑成像，使用最多三个时间点数据进行情绪行为结果数据， 我们将研究基因与环境的相互作用如何影响大脑大小和功能的变化。 2 将检验个人收入与需求之间的独立和交互影响以及多基因风险 抑郁症对大脑功能连接和先前相关的关键情绪区域的大脑结构的影响 目标 3 将进一步测试收入与需求和多基因风险评分是否相关。 最终，该项目的研究结果有可能 识别潜在的大脑行为生物标志物，这些生物标志物在确定早发风险时可能很重要 抑郁症，最终有助于改善早期发现和治疗。