Impaired neural habituation to neutral faces in families genetically enriched for social anxiety disorder
Impaired neural habituation to neutral faces in families genetically enriched for social anxiety disorder
复制标题
DOI：
10.1002/da.22962
复制
发表时间：
2019-10-10
影响因子：
7.4
通讯作者：
Westenberg, P. Michiel
中科院分区：
文献类型：
--
作者：
Bas-Hoogendam, Janna M.;van Steenbergen, Henk;Westenberg, P. Michiel
社交焦虑障碍（Social anxiety disorder， SAD）是一种家族性失能性障碍。先前的研究将社交恐惧与无法适应联系起来，但到目前为止，还没有研究SAD患者及其家庭成员对中性面孔的习惯反应。在这里，我们通过使用来自Leiden家庭实验室对SAD的多代和多代研究数据，研究了对中性面孔的习惯受损是否是SAD的一种假定的神经生物学内表型。方法参与者（n = 110，年龄9.2 - 61.5岁）进行了涉及中性面孔的习惯化范式，因为这些面孔是具有模糊含义的强烈社会刺激。我们使用功能性磁共振成像数据来调查与习惯化相关的大脑激活是否与家庭中的社交焦虑水平有关。此外，还估计了神经适应反应的遗传力。结果在右侧海马区和右侧杏仁核区发现中性面孔习惯障碍与社交焦虑之间的关系。此外，我们的数据表明，这种习惯化反应在右侧海马体中表现出中等至中等高的遗传性。结论习惯化改变是SAD的一种候选内表型；神经居住功能受损与家族内疾病共分离，具有遗传性。这些发现揭示了SAD的遗传易感性。
Background Social anxiety disorder (SAD) is an incapacitating disorder running in families. Previous work associated social fearfulness with a failure to habituate, but the habituation response to neutral faces has, as of yet, not been investigated in patients with SAD and their family members concurrently. Here, we examined whether impaired habituation to neutral faces is a putative neurobiological endophenotype of SAD by using data from the multiplex and multigenerational Leiden Family Lab study on SAD. Methods Participants (n = 110; age, 9.2 - 61.5 years) performed a habituation paradigm involving neutral faces, as these are strong social stimuli with an ambiguous meaning. We used functional magnetic resonance imaging data to investigate whether brain activation related to habituation was associated with the level of social anxiety within the families. Furthermore, the heritability of the neural habituation response was estimated. Results Our data revealed a relationship between impaired habituation to neutral faces and social anxiety in the right hippocampus and right amygdala. In addition, our data indicated that this habituation response displayed moderate - to-moderately high heritability in the right hippocampus. Conclusion The present results provide support for altered habituation as a candidate SAD endophenotype; impaired neural habitation cosegregrated with the disorder within families and was heritable. These findings shed light on the genetic susceptibility to SAD.