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A systematic review of childhood maltreatment and DNA methylation: candidate gene and epigenome-wide approaches.儿童虐待与 DNA 甲基化的系统综述:候选基因与全基因组表观遗传研究方法。
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SSTR4, Childhood Adversity, Self-efficacy and Suicide Risk in Alcoholics.生长抑素受体4、童年逆境、自我效能感与酗酒者的自杀风险
Transl Neurosci. 2017 Sep 14;8:76-86. doi: 10.1515/tnsci-2017-0013. eCollection 2017.
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A review of DNA methylation in depression.抑郁症中DNA甲基化的综述。
J Clin Neurosci. 2017 Sep;43:39-46. doi: 10.1016/j.jocn.2017.05.022. Epub 2017 Jun 20.
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Allelic distribution of BDNF Val66Met polymorphism in healthy Romanian volunteers.健康罗马尼亚志愿者中脑源性神经营养因子Val66Met多态性的等位基因分布
Transl Neurosci. 2016 Apr 22;7(1):31-34. doi: 10.1515/tnsci-2016-0006. eCollection 2016.
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How air pollution alters brain development: the role of neuroinflammation.空气污染如何改变大脑发育:神经炎症的作用。
Transl Neurosci. 2016 Mar 21;7(1):24-30. doi: 10.1515/tnsci-2016-0005. eCollection 2016.
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Associations Between Childhood Abuse, Posttraumatic Stress Disorder, and Implicit Emotion Regulation Deficits: Evidence From a Low-Income, Inner-City Population.童年期虐待、创伤后应激障碍与内隐情绪调节缺陷之间的关联:来自低收入城市中心人群的证据。
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Measuring mortality and the burden of adult disease associated with adverse childhood experiences in England: a national survey.衡量英国与童年不良经历相关的成人疾病死亡率和负担:一项全国性调查。
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Highly Expressed Genes within Hippocampal Sector CA1: Implications for the Physiology of Memory.海马体CA1区高表达基因:对记忆生理学的启示
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[Epigenetic cancer drugs and their role in anticancer therapy].
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Association between promoter methylation of serotonin transporter gene and depressive symptoms: a monozygotic twin study.5-羟色胺转运体基因启动子甲基化与抑郁症状的关联:一项同卵双胞胎研究。
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Shaping synaptic plasticity: the role of activity-mediated epigenetic regulation on gene transcription.塑造突触可塑性:活性介导的表观遗传调控对基因转录的作用。
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童年逆境并非酗酒者中SSTR4met的预测因素。

Childhood Adversities are not a Predictors of SSTR4met in Alcoholics.

作者信息

Berent Dominika, Pogórski Michał, Kulczycka-Wojdala Dominika, Kusideł Ewa, Macander Marian, Pawłowska Zofia

机构信息

Medical University of Warsaw, Department of Psychiatry II, Kondratowicza 8 Str., PL-03-242Warsaw, Poland.

Polish Mother's Memorial Hospital Research Institute, Department of Diagnostic Imaging, Rzgowska 281/289 Str., 93-338Lodz, Poland.

出版信息

Transl Neurosci. 2017 Oct 29;8:127-138. doi: 10.1515/tnsci-2017-0019. eCollection 2017.

DOI:10.1515/tnsci-2017-0019
PMID:29104801
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5662752/
Abstract

BACKGROUND

Genome methylation may modulate synaptic plasticity, being a potential background for mental disorder. Adverse childhood experiences (ACEs), known to be frequently reported by patients with alcohol dependence (AD), have been proposed as one of environmental inequities influencing DNA methylation. The study is aiming 1.To assess a promoter region methylation in gene for somatostatin receptor subtype-4 (), a receptor for somatostatin, a neurotransmitter engaged in neuroplasticity and memory formation, in patients with AD; 2. To verify if promoter methylation is associated with ACEs and other selected environmental factors. Methodology: 176 patients with AD and 127 healthy controls were interviewed regarding 13 categories of ACEs; a structured self-reported questionnaire - to measure the sociodemographic and clinical characteristics; a module of Catalogue of Healthy Behavior - to assess nutritional health habits; the Alcohol Use Disorders Identification Test - to assess drinking severity. The promoter region methylation status was performed via methylation-specific PCR, and the genotyping for the rs2567608 functional polymorphism - according to the manufacturer's standard PCR protocol.

RESULTS

promoter region was found methylated in 21.6% patients with AD and 2.3% controls. None of following characteristics: current age, gender, term and kind of labor, 13 categories of childhood trauma, diet, alcohol drinking severity, age at alcohol drinking initiation, age at onset of problem drinking, cigarette smoking, and rs2567608 was a significant predictor for promoter region methylation.

CONCLUSIONS

promoter region methylation in here studied participants may be either inherited epigenetic modification or secondary, but not to here assessed variables.

摘要

背景

基因组甲基化可能调节突触可塑性,是精神障碍的潜在背景。不良童年经历(ACEs),酒精依赖(AD)患者经常报告有此经历,已被认为是影响DNA甲基化的环境因素之一。本研究旨在:1.评估AD患者中生长抑素受体亚型4()基因启动子区域甲基化情况,生长抑素是一种参与神经可塑性和记忆形成的神经递质的受体;2.验证启动子甲基化是否与ACEs及其他选定的环境因素相关。方法:对176例AD患者和127名健康对照者进行了关于13类ACEs的访谈;使用结构化的自我报告问卷来测量社会人口统计学和临床特征;使用健康行为目录模块来评估营养健康习惯;使用酒精使用障碍识别测试来评估饮酒严重程度。通过甲基化特异性PCR检测启动子区域甲基化状态,并根据制造商的标准PCR方案对rs2567608功能多态性进行基因分型。

结果

在21.6%的AD患者和2.3%的对照者中发现启动子区域甲基化。以下特征:当前年龄、性别、劳动期限和类型、13类童年创伤、饮食、饮酒严重程度、开始饮酒年龄、问题饮酒开始年龄、吸烟以及rs2567608,均不是启动子区域甲基化的显著预测因素。

结论

本研究参与者中启动子区域甲基化可能是遗传的表观遗传修饰或继发性的,但与这里评估的变量无关。