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Addiction, Anhedonia, and Comorbid Mood Disorder. A Narrative Review.成瘾、快感缺失与共病情绪障碍。一篇叙述性综述。
Front Psychiatry. 2019 May 22;10:311. doi: 10.3389/fpsyt.2019.00311. eCollection 2019.
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Effect of Acute Stress on the Expression of BDNF, trkB, and PSA-NCAM in the Hippocampus of the Roman Rats: A Genetic Model of Vulnerability/Resistance to Stress-Induced Depression.急性应激对罗曼大鼠海马脑源性神经营养因子、trkB 和 PSA-NCAM 表达的影响:应激诱导抑郁易感性/抗性的遗传模型。
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Brain-derived neurotrophic factor in substance use disorders: A systematic review and meta-analysis.脑源性神经营养因子在物质使用障碍中的作用:系统评价和荟萃分析。
Drug Alcohol Depend. 2018 Dec 1;193:91-103. doi: 10.1016/j.drugalcdep.2018.08.036. Epub 2018 Oct 12.
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Shared genetic etiology between alcohol dependence and major depressive disorder.酒精依赖与重度抑郁症之间的共同遗传病因。
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The effect of enriched environment across ages: A study of anhedonia and BDNF gene induction.丰富环境对不同年龄段的影响:一项关于快感缺乏和脑源性神经营养因子基因诱导的研究。
Genes Brain Behav. 2018 Nov;17(8):e12485. doi: 10.1111/gbb.12485. Epub 2018 May 31.
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Molecular role of dopamine in anhedonia linked to reward deficiency syndrome (RDS) and anti- reward systems.多巴胺在与奖赏缺乏综合征(RDS)及抗奖赏系统相关的快感缺失中的分子作用。
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Cortical Expression of the Polysialylated Isoform of the Neural Cell Adhesion Molecule on Brain Tissue to Recognize Drug-Related Death: An Exploratory Analysis.神经细胞黏附分子多唾液酸化异构体在脑组织上的皮质表达以识别与药物相关的死亡:一项探索性分析。
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The role of the habenula in the transition from reward to misery in substance use and mood disorders.缰核对物质使用和情绪障碍中从奖励到痛苦的转变的作用。
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探索脑源性神经营养因子和细胞黏附分子作为酒精使用障碍和共病抑郁症中跨诊断症状快感缺乏的生物标志物。

Exploring Brain Derived Neurotrophic Factor and Cell Adhesion Molecules as Biomarkers for the Transdiagnostic Symptom Anhedonia in Alcohol Use Disorder and Comorbid Depression.

作者信息

Levchuk Lyudmila A, Meeder Elise M G, Roschina Olga V, Loonen Anton J M, Boiko Anastasiia S, Michalitskaya Ekaterina V, Epimakhova Elena V, Losenkov Innokentiy S, Simutkin German G, Bokhan Nikolay A, Schellekens Arnt F A, Ivanova Svetlana A

机构信息

Mental Health Research Institute, Tomsk National Research Medical Center of the Russian Academy of Sciences, Tomsk, Russia.

Department of Psychiatry, Donders Institute for Brain, Cognition, and Behavior, Radboudumc, Nijmegen, Netherlands.

出版信息

Front Psychiatry. 2020 Apr 20;11:296. doi: 10.3389/fpsyt.2020.00296. eCollection 2020.

DOI:10.3389/fpsyt.2020.00296
PMID:32372985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7184244/
Abstract

BACKGROUND

Alcohol Use Disorder (AUD) and depressive disorder often co-exist and have a shared heritability. This study aimed to investigate Brain-Derived Neurotrophic Factor (BDNF) and three Cell Adhesion Molecules (CAMs) as transdiagnostic biomarkers in AUD and depression co-morbidity.

METHODS

In a cross-sectional study, patients with AUD (n=22), AUD and depression (n=19), and healthy controls (n=20) were examined. Depression and anxiety severity were assessed using the Hamilton Depression Rating Scale and the Hamilton Anxiety Rating Scale. Anhedonia, alcohol use and dependence, craving, and social adaptation were assessed through self-report questionnaires. BDNF and CAM concentrations in peripheral serum were measured after overnight fasting using a Luminex assay. After controlling for age and gender, biomarker levels were compared across groups. The association between biomarker concentrations and symptom severity scales were explored using correlation and multiple regression analyses.

RESULTS

BDNF and Neuronal CAM were lower in patients with AUD with and without depression compared to healthy controls. No differences were observed for Vascular CAM-1 and Interstitial CAM-1. BDNF correlated negatively with anhedonia levels. BDNF, age and gender together explained 21% of variability in anhedonia levels.

CONCLUSION

This pilot study suggests that peripheral levels of BDNF and NCAM might be reduced in AUD with and without comorbid mood disorder. Since low BDNF levels were associated with self- reported anhedonia across these conditions, BDNF and anhedonia might reflect transdiagnostic aspects involved in AUD and depression.

摘要

背景

酒精使用障碍(AUD)和抑郁症常共存且具有共同的遗传易感性。本研究旨在调查脑源性神经营养因子(BDNF)和三种细胞黏附分子(CAMs)作为AUD与抑郁症共病的跨诊断生物标志物。

方法

在一项横断面研究中,对AUD患者(n = 22)、AUD合并抑郁症患者(n = 19)和健康对照者(n = 20)进行了检查。使用汉密尔顿抑郁量表和汉密尔顿焦虑量表评估抑郁和焦虑严重程度。通过自我报告问卷评估快感缺失、酒精使用和依赖、渴望及社会适应情况。过夜禁食后,采用Luminex分析法测量外周血清中BDNF和CAM的浓度。在控制年龄和性别后,比较各组生物标志物水平。使用相关性和多元回归分析探讨生物标志物浓度与症状严重程度量表之间的关联。

结果

与健康对照相比,患有和未患有抑郁症的AUD患者的BDNF和神经元CAM较低。血管细胞黏附分子-1和间质细胞黏附分子-1未观察到差异。BDNF与快感缺失水平呈负相关。BDNF、年龄和性别共同解释了快感缺失水平21%的变异性。

结论

这项初步研究表明,无论是否合并情绪障碍,AUD患者外周血BDNF和NCAM水平可能会降低。由于在这些情况下低BDNF水平与自我报告的快感缺失有关,BDNF和快感缺失可能反映了AUD和抑郁症中涉及的跨诊断方面。