Department of Psychology, University of Wisconsin-Madison.
Department of Biostatistics and Medical Informatics, University of Wisconsin-Madison.
J Psychopathol Clin Sci. 2022 Aug;131(6):567-574. doi: 10.1037/abn0000659.
There is substantial heterogeneity in the development of depression from adolescence into adulthood. Yet, little is known about the risk factors underlying its various patterns of development. For instance, despite the discovery of genetic variants for depression, these discoveries have not accounted for the high degree of genetic covariation between multiple disorders, nor have they been applied to disambiguate its heterogeneous developmental presentations. This study examined the association between a transdiagnostic polygenic score for psychopathology (p-factor PGS) and depression trajectories, spanning early adolescence into adulthood, in the National Longitudinal Study of Adolescent to Adult Health (N = 7,088). We examined whether subconstructs of the Research Domain Criteria's (RDoC) negative valence (i.e., negative emotionality), positive valence (i.e., novelty seeking), and cognitive systems (i.e., picture vocabulary) could explain how the p-factor PGS eventuates into the various pathways of depression. Four trajectories were identified: low depression (78.9%), low increasing (7.3%), high declining (8.2%), and early adult peaked (5.7%). The p-factor PGS was significantly higher in all depressive trajectories relative to the low-depression trajectory but was predictive of only the trajectory that showed increasing depression over time: low increasing. A specific indirect path emerged by which the association of p-factor PGS on early adult peaked and high-declining depression operated through the effects of negative emotionality but not picture vocabulary or novelty seeking. Findings reinforce the crucial role of development in genetically informed RDoC models of depression, because there appear to be distinct correlates and risk factors that underlie the various developmental pathways of depression. (PsycInfo Database Record (c) 2022 APA, all rights reserved).
从青春期到成年，抑郁症的发展存在很大的异质性。然而，人们对导致其各种发展模式的风险因素知之甚少。例如，尽管已经发现了抑郁症的遗传变异，但这些发现并没有解释多种疾病之间高度的遗传相关性，也没有用于区分其异质的发展表现。本研究在国家青少年至成人健康纵向研究（N=7088）中，考察了精神病理学的跨诊断多基因评分（p 因子 PGS）与从青春期到成年的抑郁轨迹之间的关联。我们研究了 RDoC 的负性情绪（即负性情绪）、正性情绪（即寻求新奇）和认知系统（即图片词汇）的亚结构是否可以解释 p 因子 PGS 如何导致各种抑郁途径。确定了四种轨迹：低抑郁（78.9%）、低递增（7.3%）、高递减（8.2%）和早期成人高峰（5.7%）。与低抑郁轨迹相比，所有抑郁轨迹中的 p 因子 PGS 都显著更高，但仅与随时间增加抑郁的轨迹（低递增）相关。p 因子 PGS 对早期成人高峰和高递减抑郁的关联通过负性情绪的影响，但不是图片词汇或寻求新奇的影响，出现了特定的间接路径。研究结果强化了发展在基于遗传的 RDoC 抑郁症模型中的关键作用，因为似乎存在不同的相关性和风险因素，这些因素是导致抑郁症各种发展途径的基础。（PsycInfo 数据库记录（c）2022 APA，保留所有权利）。
