ISSN 0439-755X
CN 11-1911/B
主办:中国心理学会
   中国科学院心理研究所
出版:科学出版社

心理学报 ›› 2023, Vol. 55 ›› Issue (10): 1620-1636.doi: 10.3724/SP.J.1041.2023.01620

• 研究报告 • 上一篇    下一篇

BDNF基因、同伴关系与青少年早期抑郁:基于动态发展视角

曹衍淼, 方惠慈, 朱欣悦, 纪林芹, 张文新()   

  1. 山东师范大学心理学院, 济南 250014
  • 收稿日期:2022-10-28 发布日期:2023-07-26 出版日期:2023-10-25
  • 通讯作者: 张文新, E-mail: zhangwenxin@sdnu.edu.cn
  • 基金资助:
    国家自然科学基金项目(32071073);国家自然科学基金项目(31900776);国家自然科学基金项目(31971008)

Associations among brain-derived neurotrophic factor gene, peer relationships, and depression across early adolescence: Dynamic genetic effects

CAO Yanmiao, FANG Huici, ZHU Xinyue, JI Linqin, ZHANG Wenxin()   

  1. School of Psychology, Shandong Normal University, Jinan 250014, China
  • Received:2022-10-28 Online:2023-07-26 Published:2023-10-25

摘要:

青少年抑郁是遗传基因与环境动态交互作用的结果, 但是现有研究忽视了抑郁遗传效应的发展动态性。本研究通过对1086名青少年(平均年龄12.32, 50%女生)进行3年的追踪, 分别从遗传效应的年龄差异以及遗传效应影响抑郁发展轨迹的角度, 考察BDNF基因与同伴关系对青少年抑郁的动态影响。结果显示:(1)在3个时间点上, BDNF基因与同伴拒绝交互影响青少年抑郁, 但其作用模式存在年龄差异:12岁时, MetMet基因型携带者对环境敏感性高于ValMet基因型携带者; 13岁时, MetMet和ValVal基因型携带者对环境的敏感性均高于ValMet基因型携带者; 14岁时, ValVal基因型携带者对环境的敏感性高于ValMet基因型携带者。(2)青少年早期抑郁呈线性增长趋势, 但是抑郁初始水平与增长速度无关。(3) BDNF基因与同伴拒绝交互预测青少年抑郁的初始水平, 相比ValMet基因型, 携带MetMet基因型的青少年在经历同伴拒绝后抑郁初始水平更高。(4) BDNF基因显著预测青少年抑郁增长速度, 相比ValMet基因型携带者, 携带MetMet和ValVal基因型的青少年抑郁增长速度更快。

关键词: 青少年抑郁, BDNF基因, 同伴拒绝, 年龄差异, 潜变量增长模型

Abstract:

There has been a dramatic rise in gene-environment interaction (G × E) studies of depression over the last two decades. These studies are pivotal to understanding the etiology of depression and individual differences in environmental sensitivity. However, these studies rarely take into consideration how the genotype by environment interactions change over development and how the interactions work on the developmental trajectories of depression. The brain-derived neurotrophic factor (BDNF) gene is a good candidate for the investigation of the dynamic genetic effects on depression because it is involved in several age-related changes in behavior and brain maturation. On the one hand, the effect of the BDNF gene may depend on the basal BDNF level. The BDNF level peaks during adolescence, so the effect of the BDNF gene on depression may change during development. Moreover, peer experiences change may alter epigenetic modifications of the BDNF gene, which may change the pattern of gene-environment interactions. On the other hand, according to the developmental cascades model, the differences in genetic effects on depression may increase over time in that initial depressive symptoms may evoke poor peer experiences. Taken together, this study aimed to investigate the age differences in the G × E interaction on depression and the G × E effect on the developmental trajectories of depression.

One thousand and eighty-six adolescents (aged 11-12 years with a mean of 12.32, 50% girls) were followed up for three years. Saliva samples, self-reported depressive symptoms, and peer nomination were all collected. All of the measures showed good reliability. Concurrent hierarchical regression analyses and latent growth curve models (LGCMs) were conducted. We also completed re-parameterized regression and parallel LGCMs to understand the gene by environment interaction pattern and the dynamic association between peer relationships and depression.

The results showed that the BDNF Val66Met polymorphism significantly moderated the influence of peer rejection—but not peer acceptance—on youth depressive symptoms at three time points; however, the susceptible genotype changed over time. In particular, the effect of peer rejection on depression was stronger in MetMet compared to ValMet carriers at 12 years of age; the effect of peer rejection on depression was stronger in MetMet and ValVal compared to ValMet carriers at 13 years of age; the effect of peer rejection on depression was stronger in ValVal carriers compared to ValMet carriers at 14 years of age. LGCMs suggested that adolescents’ depression increased in a linear trajectory from 12 to 14 years of age. In addition, there were significant genotype differences in the change of depression over time, but this effect was not moderated by peer relationships.

These findings may move research in the field away from the simplistic notion of risk alleles, recognizing that an allele may be a risk factor during one period and a protective factor during another. Further, this study has progressed the conceptualization of how genes and the environment interact to influence the developmental trajectories of depression during early adolescence.

Key words: adolescent depression, BDNF, peer rejection, age differences, latent growth curve model

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