Stoychev Kaloyan, Dilkov Dancho, Naghavi Elahe, Kamburova Zornitsa
Department of Psychiatry, Medical University Pleven, 5800 Pleven, Bulgaria.
Department of Psychiatry, Military Medical Academy Sofia, 1606 Sofia, Bulgaria.
Diagnostics (Basel). 2021 Jun 8;11(6):1055. doi: 10.3390/diagnostics11061055.
(1) Background: Comorbidity between Alcohol Use Disorders (AUD), mood, and anxiety disorders represents a significant health burden, yet its neurobiological underpinnings are elusive. The current paper reviews all genome-wide association studies conducted in the past ten years, sampling patients with AUD and co-occurring mood or anxiety disorder(s). (2) Methods: In keeping with PRISMA guidelines, we searched EMBASE, Medline/PUBMED, and PsycINFO databases (January 2010 to December 2020), including references of enrolled studies. Study selection was based on predefined criteria and data underwent a multistep revision process. (3) Results: 15 studies were included. Some of them explored dual diagnoses phenotypes directly while others employed correlational analysis based on polygenic risk score approach. Their results support the significant overlap of genetic factors involved in AUDs and mood and anxiety disorders. Comorbidity risk seems to be conveyed by genes engaged in neuronal development, connectivity, and signaling although the precise neuronal pathways and mechanisms remain unclear. (4) Conclusion: given that genes associated with complex traits including comorbid clinical presentations are of small effect, and individually responsible for a very low proportion of the total variance, larger samples consisting of multiple refined comorbid combinations and confirmed by re-sequencing approaches will be necessary to disentangle the genetic architecture of dual diagnosis.
(1)背景:酒精使用障碍(AUD)与情绪及焦虑障碍之间的共病构成了重大的健康负担,但其神经生物学基础尚不清楚。本文回顾了过去十年中开展的所有全基因组关联研究,这些研究对患有AUD以及同时患有情绪或焦虑障碍的患者进行了抽样。(2)方法:按照PRISMA指南,我们检索了EMBASE、Medline/PUBMED和PsycINFO数据库(2010年1月至2020年12月),包括纳入研究的参考文献。研究选择基于预定义标准,数据经过多步骤修订过程。(3)结果:纳入了15项研究。其中一些研究直接探讨了双重诊断表型,而其他研究则采用基于多基因风险评分方法的相关性分析。他们的结果支持了AUD与情绪及焦虑障碍所涉及的遗传因素存在显著重叠。共病风险似乎由参与神经元发育、连接和信号传导的基因传递,尽管确切的神经元途径和机制仍不清楚。(4)结论:鉴于与包括共病临床表现在内的复杂性状相关的基因效应较小,且各自对总变异的贡献率非常低,因此需要更大规模的样本,这些样本由多种精细的共病组合组成,并通过重测序方法进行确认,以厘清双重诊断的遗传结构。