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.

项目摘要 /摘要 抑郁症是全球疾病烧伤的主要因素之一，世界卫生组织 （谁）将其排名为第一名的非致命贡献者。大多数抑郁案出现 生命的第三十年，被归类为早期抑郁症。早期抑郁症的长期影响 延伸到成年期，通常会导致较高的复发率和重大健康问题。研究 已经表明，疾病发作之前的早期干预会带来最佳结果。因此，提早检测 抑郁症风险的标志将有助于减轻疾病。以前的调查研究了 环境暴露或遗传影响分别，研究开始检查互动 基因和环境对抑郁症风险的影响。但是，很少有研究检查 逐个环境的基因相互作用如何映射到原始人的大脑和早期风险的行为生物标志物上 发作抑郁症，这可以极大地帮助早期检测和治疗。具体而言，选择大脑结构 和功能网络以及独特的情感行为（例如积极影响和撤回） 症状 - 一直与早期发作抑郁症保持联系。最终，这表明这些 研究基因逐个环境可能会导致抑郁症的风险，可能是重要的生物标志物 出现在疾病发作之前。那是这项研究将检查众所周知的环境预测因子 家庭收入到需要的人可能具有独立和/或互动效果以及个人的多基因 抑郁症的风险评分在情绪大脑结构和功能从前到早期发育的发展 青少年。为了实现这一目标，当前的研究将利用现有的纵向数据 在基线时约有5,000名9-10岁的受试者，到11-12岁的年龄在2年的随访中 在整个美国，作为较大的青少年大脑认知发展的一部分？研究（ABCD研究®）。 使用两个时间点数据进行大脑成像，最多三个时间点用于情感行为结果数据， 我们将研究基因与环境相互作用如何影响大脑大小和功能的变化。目标1并瞄准 2将检查一个人的收入和多基因风险的独立和互动效果 对功能性大脑连通性和关键情绪区域的大脑结构的抑郁症先前相关 分别有抑郁症。 AIM 3将进一步测试收入到需求和多基因风险评分与 建立的前途情感行为。最终，该项目的发现有可能 确定潜在的脑行为生物标志物，这些生物标志物在建立早期发作风险时可能很重要 抑郁症，最终有助于改善早期检测和治疗。