Lehto Kelli, Mäestu Jarek, Kiive Evelyn, Veidebaum Toomas, Harro Jaanus
Division of Neuropsychopharmacology, Department of Psychology, Estonian Centre of Behavioural and Health Sciences, University of Tartu, Ravila 14A, 50411 Tartu, Estonia; National Institute for Health Development, Estonian Centre of Behavioural and Health Sciences, Tallinn, Estonia.
Department of Sports Biology and Physiotherapy, Estonian Centre of Behavioural and Health Sciences, University of Tartu, Tartu, Estonia.
Eur Neuropsychopharmacol. 2016 Mar;26(3):562-9. doi: 10.1016/j.euroneuro.2015.12.029. Epub 2015 Dec 19.
The brain-derived neurotrophic factor gene (BDNF) Val66Met polymorphism and life stress have been associated with negative emotionality (e.g., neuroticism), but relevant evidence is far from unequivocal. Possible confounding factors include the type and timing of stressful events measured, such as childhood adversity vs. recent stressful events, and variable gene × environment interactions. The aim of this study was to longitudinally assess the BDNF Val66Met polymorphism and environment interaction effect on neuroticism in a population representative sample, depending upon the type of stress, gender and family relations. In the original older cohort of the Estonian Children Personality Behavior and Health Study (ECPBHS, n=593), neuroticism was measured at age 15 (parental assessment), 18 and 25 (self-assessments). Childhood stress was reported at age 15, quality of family relations was measured at age 18, and recent stressful life events at age 25. The BDNF Val66Met polymorphism interacted with recent stressful life events, but not with childhood adversities, to impact neuroticism. Interestingly, in female participants, neuroticism at age 18 predicted future stressful life events dependent upon genotype: individuals with Val/Val genotype and high neuroticism experienced higher, but Met-allele carriers with high neuroticism lower stress exposure at age 25. Similar tendencies were observed using parental assessments at age 15. The protective effect of Met-allele in the high stress exposure group could result from better early family environment. In conclusion, we herewith provide further evidence for a role of BDNF gene variance contributing to plasticity in response to environmental demands.
脑源性神经营养因子基因（BDNF）Val66Met多态性与生活压力一直与负面情绪（如神经质）有关，但相关证据远未明确。可能的混杂因素包括所测量的应激事件的类型和时间，如童年逆境与近期应激事件，以及基因×环境相互作用的变异性。本研究的目的是在一个具有代表性的人群样本中，根据应激类型、性别和家庭关系，纵向评估BDNF Val66Met多态性与环境对神经质的交互作用。在爱沙尼亚儿童个性行为与健康研究（ECPBHS，n = 593）最初的老年队列中，在15岁（父母评估）、18岁和25岁（自我评估）时测量神经质。在15岁时报告童年应激，在18岁时测量家庭关系质量，在25岁时测量近期应激生活事件。BDNF Val66Met多态性与近期应激生活事件相互作用，但与童年逆境无关，从而影响神经质。有趣的是，在女性参与者中，18岁时的神经质根据基因型预测未来的应激生活事件：Val/Val基因型且神经质高的个体经历的应激更高，但携带Met等位基因且神经质高的个体在25岁时经历的应激更低。在15岁时使用父母评估也观察到了类似趋势。Met等位基因在高应激暴露组中的保护作用可能源于更好的早期家庭环境。总之，我们在此提供了进一步的证据，证明BDNF基因变异在响应环境需求时对可塑性的作用。
