Wilker Sarah, Elbert Thomas, Kolassa Iris-Tatjana
Clinical & Biological Psychology, Institute of Psychology & Education, University of Ulm, Albert-Einstein-Allee 47, 89069 Ulm, Germany.
Clinical Psychology & Neuropsychology, University of Konstanz, Universitätsstr. 10, 78457 Konstanz, Germany.
Neurobiol Learn Mem. 2014 Jul;112:75-86. doi: 10.1016/j.nlm.2013.08.015. Epub 2013 Sep 4.
A good memory for emotionally arousing experiences may be intrinsically adaptive, as it helps the organisms to predict safety and danger and to choose appropriate responses to prevent potential harm. However, under conditions of repeated exposure to traumatic stressors, strong emotional memories of these experiences can lead to the development of trauma-related disorders such as posttraumatic stress disorder (PTSD). This syndrome is characterized by distressing intrusive memories that can be so intense that the survivor is unable to discriminate past from present experiences. This selective review on the role of memory-related genes in PTSD etiology is divided in three sections. First, we summarize studies indicating that the likelihood to develop PTSD depends on the cumulative exposure to traumatic stressors and on individual predisposing risk factors, including a substantial genetic contribution to PTSD risk. Second, we focus on memory processes supposed to be involved in PTSD etiology and present evidence for PTSD-associated alterations in both implicit (fear conditioning, fear extinction) and explicit memory for emotional material. This is supplemented by a brief description of structural and functional alterations in memory-relevant brain regions in PTSD. Finally, we summarize a selection of studies indicating that genetic variations found to be associated with enhanced fear conditioning, reduced fear extinction or better episodic memory in human experimental studies can have clinical implications in the case of trauma exposure and influence the risk of PTSD development. Here, we focus on genes involved in noradrenergic (ADRA2B), serotonergic (SLC6A4), and dopaminergic signaling (COMT) as well as in the molecular cascades of memory formation (PRKCA and WWC1). This is supplemented by initial evidence that such memory-related genes might also influence the response rates of exposure-based psychotherapy or pharmacological treatment of PTSD, which underscores the relevance of basic memory research for disorders of altered memory functioning such as PTSD.
对引发情绪的经历拥有良好记忆可能具有内在适应性，因为它有助于生物体预测安全与危险，并选择适当反应以预防潜在伤害。然而，在反复暴露于创伤性应激源的情况下，对这些经历的强烈情绪记忆会导致创伤后应激障碍（PTSD）等创伤相关障碍的发生。该综合征的特征是令人痛苦的侵入性记忆，其强度可能大到幸存者无法区分过去与当下的经历。这篇关于记忆相关基因在PTSD病因学中作用的选择性综述分为三个部分。首先，我们总结研究表明，患PTSD的可能性取决于对创伤性应激源的累积暴露以及个体的易感风险因素，包括PTSD风险有很大的遗传因素。其次，我们聚焦于推测参与PTSD病因学的记忆过程，并展示PTSD与内隐（恐惧条件作用、恐惧消退）和外显情绪材料记忆改变相关的证据。PTSD中与记忆相关脑区的结构和功能改变的简要描述对此进行了补充。最后，我们总结一系列研究表明，在人类实验研究中发现与增强恐惧条件作用、减少恐惧消退或更好的情景记忆相关的基因变异，在创伤暴露情况下可能具有临床意义，并影响PTSD发生的风险。在此，我们聚焦于参与去甲肾上腺素能（ADRA2B）、5-羟色胺能（SLC6A4）和多巴胺能信号传导（COMT）以及记忆形成分子级联反应（PRKCA和WWC1）的基因。此类与记忆相关基因也可能影响基于暴露的心理治疗或PTSD药物治疗的反应率的初步证据对此进行了补充，这凸显了基础记忆研究对于记忆功能改变的障碍如PTSD的相关性。
