暨南大学附属第一医院贾艳滨学术不端投诉

被投诉单位：暨南大学附属第一医院

被投诉人： 贾艳滨

被投诉文章：“创伤后应激障碍影像遗传学研究进展”，中国神经精神疾病杂志 2019 年 第45 卷 第 8 期

“创伤后应激障碍影像遗传学研究进展”这个稿件基本是翻译于“Neuroimaging genetic approaches to Posttraumatic Stress Disorder”。稿件里面每一个元素要点都能在原文中找到，而且原文发表于Exp Neurol期刊。参考文献当中第一个也是Exp Neurol期刊。著者不可能没有看过。

该文

分子伴侣 FK506 结合蛋白 5（FK506-binding protein 5，FKBP5） 基 因 影 像 学 研 究 FKBP5 基 因 rs9296158 、 rs3800373、rs1360780 和 rs9470080 是 PTSD 的 风 险 基 因 ， 且与应激反应增强及 PTSD 症状严重程度相关。 静息态功 能磁共振成像 （functional magnetic resonance imaging，fMRI） 研究发现健康人群中，风险基因携带者的额颞顶叶网络区 域功能连接性较差，更易受严重应激反应影响[5]。 任务态 fMRI 研究也发现，在面对威胁刺激时，rs1360780 T 型基因 携带者的左侧海马和海马旁回脑区激活高于 C 型基因携 带者[6]。 结合弥散张量成像（diffusion tensor imaging，DTI）和 MRI 研究发现， 经历过创伤的成年女性 rs1360780 T 型基 因 携 带 者 左 后 侧 扣 带 回 的 各 向 异 性 指 数 （fractional anisotropy，FA）值、前扣带回皮层与海马间的功能连接明显 低于 C 型基因携带者，且与注意及记忆功能关联[7-9]。 基于 全脑体素的 MRI 研究发现，与正常对照相比，经历过创伤 的 rs1360780 TT 型儿童大脑灰质体积减少， 包括双侧岛 叶、颞上回和颞中回、双侧海马、右侧杏仁核和双侧前扣带 皮层等区域，与经历过创伤的 CT/CC 型儿童相比，TT 型儿 童右侧海马、海马旁回、双侧前中扣带皮层、脑岛和杏仁核 体积显著减少， 该研究结果提示 rs1360780 和童年创伤的 相互作用与脑结构改变有关，如海马、扣带皮层、杏仁核等 脑区，而以上脑区在情感过程中起关键作用[10]。 此外，尸检 研究发现 PTSD 患者膝下前额叶皮层的 FKBP5 基因表达 水平下降[11]。 FKBP5 基因多态性及其表达异常可能会导致 额叶、扣带回和海马等脑区结构及功能异常，严重影响患 者情绪处理和认知功能。

认为剽窃原文中的

FKBP5—FK506-binding protein 5 gene (FKBP5) modulates glucocorticoid receptor activity (Zannas et al., 2016). Increases in the protein produced by this gene inhibit glucocorticoid signaling either by decreasing the sensitivity or increasing the resistance of the receptor (Zannas et al., 2016). FKBP5 is highly expressed in the hippocampus (Zannas et al., 2016), a structure involved in memory for consciously recalled events (declarative/ explicit memory; Kim & Diamond, 2002; Squire, 1992). During memory formation the hippocampus (HP) helps bind together patterns of neural activity throughout the brain that comprise an episodic memory (Kim & Diamond, 2002; Squire, 1992). The SNP rs1360780 risk allele (T) is associated with increased FKBP5 transcription, and therefore increased inhibition of glucocorticoid signaling (Zannas et al., 2016). Interestingly, low glucocorticoid levels and reduced glucocorticoid action have been implicated as vulnerabilities toward developing PTSD (Resnick et al., 1995; Yehuda et al., 1998). In an adult sample of civilian African American women with a high trauma load, Fani et al (2013) found that FKBP5 SNP rs1360780 risk allele carriers (TT/TC) had altered left HP shape compared to nonrisk allele carriers (CC). This alteration in shape occurred especially in the CA1 region of the HP. Stress blocks neurogenesis in the HP, induces dendritic atrophy, and reduces long-term potentiation (Kim & Diamond, 2002; Sapolsky et al., 1990), which makes it a particularly vulnerable brain structure in PTSD. Approximately half of the sample had current PTSD as measured by the PTSD Symptom Scale, but this diagnosis and symptoms were not significantly different between the risk and nonrisk allele groups. Those with the risk allele (TT/TC), however, had increased attention toward threat cues on an attention task (described in detail in the fMRI section), a hallmark of PTSD symptomatology. One possible interpretation, given this cross-sectional sample, is that HP structural differences associated with increased threat bias in risk allele carries represent a vulnerability toward developing PTSD. Differential structure of the posterior cingulum has also been linked to FKBP5 SNP rs1360780. The posterior cingulum is a bundle of white matter fibers that runs from the frontal lobe (anterior cingulate) to the temporal lobe (entorhinal cortex). It is a central line of communication between structures in the temporal and frontal lobes (Fani et al., 2014). Abnormalities in the posterior cingulum imply a disruption or dysregulation in communication between these areas. In an adult African American female sample, risk allele carriers (T) had lower fractional anisotropy in the left posterior cingulum, reflecting either lower fiber density, axonal diameter, myelination, or a combination thereof, in this region (Fani et al., 2014; Figure 2A). There was no interaction between genotype, posterior cingulum fractional anisotropy, and PTSD symptoms or diagnosis (approximately half of the sample had a current PTSD diagnosis as measured by the PTSD Symptom Scale). A tentative interpretation to be drawn from this cross-sectional sample is that decreased white matter integrity of the posterior cingulum is a vulnerability toward developing PTSD.