Department of Medical Imaging, Jinling Hospital, Medical School of Nanjing University, Nanjing, Jiangsu, 210002, China.
Imaging Genetics Center, Mark and Mary Stevens Neuroimaging and Informatics Institute, University of Southern California, Marina del Rey, CA, 90292, USA.
Psychol Med. 2021 Jun;51(8):1310-1319. doi: 10.1017/S0033291720000045. Epub 2020 Jan 27.
Losing one's only child is a major traumatic life event that may lead to post-traumatic stress disorder (PTSD); however, the underlying mechanisms of its psychological consequences remain poorly understood. Here, we investigated subregional hippocampal functional connectivity (FC) networks based on resting-state functional magnetic resonance imaging and the deoxyribonucleic acid methylation of the human glucocorticoid receptor gene () in adults who had lost their only child.
A total of 144 Han Chinese adults who had lost their only child (51 adults with PTSD and 93 non-PTSD adults [trauma-exposed controls]) and 50 controls without trauma exposure were included in this fMRI study (age: 40-67 years). FCs between hippocampal subdivisions (four regions in each hemisphere: 1 [CA1], CA2, CA3, and [DG]) and methylation levels of the gene were compared among the three groups.
Trauma-exposed adults, regardless of PTSD diagnosis, had weaker positive FC between the left hippocampal CA1, left DG, and the posterior cingulate cortex, and weaker negative FC between the right CA1, right DG, and several frontal gyri, relative to healthy controls. Compared to non-PTSD adults, PTSD adults showed decreased negative FC between the right CA1 region and the right middle/inferior frontal gyri (MFG/IFG), and decreased negative FC between the right DG and the right superior frontal gyrus and left MFG. Both trauma-exposed groups showed lower methylation levels of the gene.
Adults who had lost their only child may experience disrupted hippocampal network connectivity and methylation status, regardless of whether they have developed PTSD.
失去独生子是一个重大的创伤性生活事件，可能导致创伤后应激障碍（PTSD）；然而，其心理后果的潜在机制仍知之甚少。在这里，我们研究了基于静息态功能磁共振成像和人类糖皮质激素受体基因（）脱氧核糖核酸甲基化的失去独生子的成年人的海马亚区功能连接（FC）网络。
共有 144 名汉族成年人失去了他们唯一的孩子（51 名 PTSD 成年人和 93 名非 PTSD 成年人[创伤暴露对照组]）和 50 名没有创伤暴露的对照者纳入这项 fMRI 研究（年龄：40-67 岁）。比较了三组之间海马亚区（每个半球的四个区域：1[CA1]、CA2、CA3 和 [DG]）之间的 FC 和基因的甲基化水平。
无论 PTSD 诊断如何，创伤暴露的成年人与健康对照组相比，左侧海马 CA1、左侧 DG 和后扣带皮层之间的正 FC 较弱，右侧 CA1、右侧 DG 和几个额回之间的负 FC 较弱。与非 PTSD 成年人相比，PTSD 成年人的右侧 CA1 区与右侧中/下额回（MFG/IFG）之间的负 FC 减少，以及右侧 DG 与右侧额上回和左侧 MFG 之间的负 FC 减少。两组创伤暴露者的基因甲基化水平均较低。
失去独生子的成年人可能会经历海马网络连接和基因甲基化状态的破坏，无论是否患有 PTSD。
