Pathways to Depression in Children of Depressed Mothers

虽然母亲和儿童抑郁症之间的联系已经很好地建立起来，但人们对母亲和儿童抑郁症之间的联系知之甚少。 这种风险是由什么机制造成的。拟议的研究旨在解决这一差距。这样 在做这件事的时候，我们试图整合和扩展来自两个独立研究领域的发现：认知-人际关系 抑郁症和精神遗传学的模型。拟议的研究涉及纵向调查， 从社区抽取母亲及其子女（8-14岁），每六个月进行一次评估， 两年研究将招募两组母亲：（a）有重度抑郁症病史的母亲 （b）在他们的孩子的生活中患有抑郁症（MDD）的人和（B）没有任何抑郁症的终生史的人， 目前没有I轴紊乱我们的主要目标是研究儿童认知能力的发展 易患抑郁症（消极归因风格和对面部表情的注意和解释偏见） 情绪的表现）。我们假设母亲的抑郁症病史与以下因素的存在有关： 他们的孩子会有更多的消极认知方式，这些认知方式会变得更加消极。 在随访过程中，作为母亲持续抑郁症状水平的函数。我们也 假设孩子生活中的负面事件（母亲的批评以及一般的负面事件） 事件）将预测儿童认知风格的负面变化。综合最近的调查结果， 精神病遗传学，我们预测，这些影响儿童的认知风格将缓和两个 特定的遗传风险因素-5-羟色胺转运体基因（5-HTTLPR）的功能多态性， 脑源性神经营养因子（BDNF）基因的候选多态性。我们的第二个目标是 测试一个连接母亲和儿童抑郁症的交易认知-人际中介模型。在 测试这个模型，我们假设，与对照组母亲相比，有MDD病史的母亲， 在随访期间表现出抑郁症状的升高水平。这些抑郁症状 假设海拔高度有助于儿童生活中负面事件的发生，这将 进而促进儿童消极认知方式的发展。这些消极的认知方式， 然后，假设有助于儿童的症状和抑郁症的诊断。建筑从 压力产生的文献，我们还将测试的假设，儿童的抑郁水平将 负性事件和儿童认知方式的前瞻性变化预测。我们还预计 儿童的5-HTTLPR和BDNF基因型将减轻母亲抑郁的影响， 事件，以及儿童对儿童抑郁症的认知，可以提高预测 儿童是抑郁症代际传播的最大风险。第三个目标是 检查中介模型与儿童抑郁症和其他疾病之间联系的特异性 (e.g.,焦虑和破坏性行为障碍）。

Although the link between maternal and child depression is well established, little is known about the mechanisms by which this risk is conferred. The proposed study is designed to address this gap. In so doing, we seek to integrate and extend findings from two separate lines of research: cognitive-interpersonal models of depression and psychiatric genetics. The proposed study involves a longitudinal investigation of mothers and their children (ages 8-14 years) drawn from the community and assessed every six months for two years. Two groups of mothers will be recruited for the study: (a) those with a history of major depressive disorder (MDD) during their child’s life and (b) those with no lifetime history of any depressive disorder and no current Axis I disorder. Our primary goal is to examine the development of children’s cognitive vulnerability to depression (negative attributional style and attention and interpretation biases for facial displays of emotion). We hypothesize that maternal history of MDD will be associated with the presence of more negative cognitive styles in their children and that these cognitive styles will become more negative over the course of the follow-up as a function of mother’s ongoing depressive symptom levels. We also hypothesize that negative events in the children’s lives (maternal criticism as well as general negative events) will predict negative changes in children’s cognitive styles. Integrating recent findings from psychiatric genetics, we predict that these effects on children’s cognitive styles will be moderated by two specific genetic risk factors – a functional polymorphism in the serotonin transporter gene (5-HTTLPR) and a candidate polymorphism in the brain-derived neurotrophic factor (BDNF) gene. Our secondary goal is to test a transactional cognitive-interpersonal mediation model linking maternal and child depression. In testing this model, we hypothesize that mothers with a history of MDD, compared to control mothers, will exhibit elevated levels of depressive symptoms across the follow-up. These depressive symptom elevations are hypothesized to contribute to the occurrence of negative events in children’s lives, which will then contribute to the development of children’s negative cognitive styles. These negative cognitive styles, then, are hypothesized to contribute to children’s symptoms and diagnoses of depression. Building from the stress-generation literature, we will also test the hypothesis that children’s levels of depression will reciprocally predict prospective changes in negative events and children’s cognitive styles. We also predict that children’s 5-HTTLPR and BDNF genotypes will moderate the impact of mother depression, negative events, and children’s cognitions upon child depression, allowing increased precision in predicting which children are at greatest risk for the intergenerational transmission of depression. A tertiary goal is to examine the specificity of the links in the mediational model to children’s depression versus other disorders (e.g., anxiety and disruptive behavior disorders).