Pathways to Depression in Children of Depressed Mothers

尽管母婴抑郁症之间的联系已经确立，但人们对抑郁症的 这种风险产生的机制。拟议的研究旨在解决这一差距。在苏中 这样做，我们寻求整合和扩展两个不同研究方向的研究结果：认知-人际关系 抑郁症和精神遗传学的模型。拟议的研究涉及一项纵向调查， 母亲及其子女(8-14岁)从社区中抽取，每六个月评估一次 两年了。这项研究将招募两组母亲：(A)有严重抑郁症病史的母亲 (B)那些一生中没有任何抑郁障碍史的人和 目前没有I型轴心紊乱。我们的主要目标是研究儿童认知能力的发展 易患抑郁症(负性归因方式和对面部的注意和解释偏差 情绪的表现)。我们假设MDD的母体病史将与 他们的孩子会有更多的负面认知风格，这些认知风格会变得更负面 在随访过程中，母亲持续的抑郁症状水平起作用。我们也 假设儿童生活中的负面事件(母性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。将最新的发现与 精神遗传学，我们预测，这些对儿童认知方式的影响将被两个方面缓和 特定的遗传风险因素-5-羟色胺转运体基因(5-HTTLPR)和 脑源性神经营养因子(BDNF)基因的候选多态性。我们的次要目标是 测试一种将母婴抑郁联系在一起的交易型认知-人际中介模型。在……里面 在测试这一模型时，我们假设有MDD病史的母亲与对照母亲相比， 在随访期间表现出抑郁症状的水平升高。这些抑郁症状 海拔高度被认为会导致儿童生活中负面事件的发生，这将 从而促进儿童消极认知风格的发展。这些消极的认知方式， 然后，被认为是导致儿童抑郁症症状和诊断的因素。从建筑开始 ，我们还将检验这样一个假设，即儿童的抑郁水平将 相互预测负面事件和儿童认知风格的预期变化。我们还预测 认为孩子的5-HTTLPR和BDNF基因型会缓和母亲抑郁的影响，为负性 事件，以及儿童对儿童抑郁的认知，从而提高了预测 儿童患抑郁症代际传播的风险最大。第三个目标是 检查中介模型中与儿童抑郁和其他障碍的联系的特异性 (例如，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).