Common and Distinct Mechanisms of Social Anxiety and Alcohol Use

社交焦虑障碍（SAD）经常与酒精使用障碍（AUD）共同发生。我们的项目旨在理清SAD和AUD的共同和特定的行为和神经元机制，以调查潜在的共享漏洞。尽管SAD与威胁反应性和绩效监控的增加有关，但研究表明，在威胁反应性或奖励敏感性和冲动性改变的情况下，患AUD的风险会增加。然而，尚不清楚这些机制的哪些改变组合与SAD和AUD的合并症有关。先前的研究表明，SAD患者中存在一种冲动性焦虑亚型，这可能解释了有问题的酒精使用，并与自我报告的奖励敏感性和冲动性有关。然而，迄今为止还没有研究调查这种合并症的潜在机制。我们将重点关注与焦虑或成瘾密切相关的标记。在无/可预测/不可预测的威胁任务中，使用肌电图评估威胁反应为惊吓反应。在功能性磁共振成像中，奖励敏感性的标志是纹状体活动和在货币激励延迟任务中的反应时间。与错误相关的消极情绪将作为绩效监测的标志，并将在侧卫任务中使用脑电图（EEG）进行评估。冲动性将用反应抑制和延迟折现来检验。脑电图中N2和P3振幅可作为神经元在停止信号任务中反应抑制的标志。在延迟折现任务中，折现因子（k值）将作为行为标记进行评估。这项多方法研究将在四组参与者中进行：患有SAD、AUD、共病SAD + AUD的个体和健康对照组。除了对每种机制进行维度和组比较分析外，我们还将进行总体潜在类分析，以检查潜在的行为和神经元机制是否可以解释SAD和AUD的合并症。这个项目的结果对于理解所检查的疾病之间的合并症高度相关，并为开发和改进针对SAD和AUD患者的定制治疗程序提供基础。

Social anxiety disorder (SAD) co-occurs frequently with alcohol use disorder (AUD). Our project aims to disentangle common and specific behavioral and neuronal mechanisms of SAD and AUD to investigate potential shared vulnerabilities. Whereas SAD is associated with increased threat reactivity and performance monitoring, the risk to develop AUD is suggested to be enhanced under either altered threat reactivity or reward sensitivity and impulsivity. However, it remains unclear which combination of alterations in these mechanisms are associated with the comorbidity of SAD and AUD. Prior work suggests that there is an impulsive-anxious subtype among individuals with SAD which might account for problematic alcohol use and is associated with self-reported reward sensitivity and impulsivity. However, no study to date has investigated underlying mechanisms regarding this comorbidity. We will focus on markers robustly associated with anxiety or addiction. Threat reactivity will be assessed as startle response using electromyography in a no/predictable/unpredictable threat task. Markers for reward sensitivity will be striatal activity and reaction times in a monetary incentive delay task during functional magnetic resonance imaging. The error-related negativity will serve as a marker for performance monitoring and will be assessed in a flanker task using electroencephalography (EEG). Impulsivity will be examined with response inhibition and delay discounting. The N2 and P3 amplitude will serve as neuronal markers of response inhibition in a stop signal task during EEG. The discounting factor (k-value) will serve as a behavioral marker assessed in a delay discounting task. This multimethod study will be conducted in four groups of participants: Individuals with SAD, AUD, comorbid SAD + AUD and healthy controls. Besides dimensional and group comparison analyses for each mechanisms, we will conduct an overall latent class analysis to examine whether underlying behavioral and neuronal mechanisms explain across and beyond diagnoses the comorbidity of SAD and AUD. The results of this project would be highly relevant for understanding the comorbidity between the examined disorders and providing a basis for developing and improving tailored treatment procedures for individuals with SAD and AUD.