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