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.

项目总结/摘要 抑郁症是全球疾病负担的主要贡献者之一，世界卫生组织 (WHO)将其列为非致命因素的第一位。大多数抑郁症病例是由个人的 第三个十年的生活，这被归类为早发性抑郁症。早发性抑郁症的长期影响 这种情况会延续到成年期，通常会导致高复发率和严重的健康问题。研究 研究表明，在疾病发作前进行早期干预可取得最佳结果。因此，及早发现 抑郁风险的标志物将有助于减轻疾病。以前的调查研究了 环境暴露或遗传影响分开，研究开始检查交互作用 基因和环境对抑郁症风险的影响。尽管如此，很少有研究 基因与环境相互作用如何映射到前驱期大脑和早期癌症风险行为生物标志物 抑郁症发作，这可以大大有助于早期发现和治疗。具体来说，选择大脑结构 和功能网络以及不同的情感行为--如积极的情感和退缩 症状-一直与早发性抑郁症有关。最终，它表明， 可能是研究基因与环境如何影响抑郁症风险的重要生物标志物， 在疾病发作之前出现。因此，本研究将探讨是否著名的环境预测 家庭收入与需求的比例可能具有独立和/或交互作用，沿着个人的多基因 抑郁症风险评分对情绪脑结构和功能发展的影响 青春期为了实现这一目标，目前的研究将利用现有的纵向数据， 约5，000例基线时9-10岁至2年随访时11-12岁的受试者， 作为更大的青少年大脑认知发展的一部分？研究（ABCD研究®）。 使用两个时间点的脑成像数据和多达三个时间点的情绪行为结果数据， 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。目标1和目标 2将研究个人的收入对需求和多基因风险的独立和交互作用， 抑郁症对功能性大脑连接和先前相关的关键情感区域的大脑结构 抑郁症，分别。目标3将进一步检验收入-需求和多基因风险评分是否相关 形成的前驱情绪行为最终，该项目的发现有可能 识别潜在的脑行为生物标志物，这些生物标志物在确定早发性脑梗死风险时可能是重要的 抑郁症，最终有助于改善早期发现和治疗。