From the neurobiological basis of comorbid alcohol dependence and depression to psychological treatment strategies: bridging the knowledge gap

据估计，酒精成瘾中情感障碍的患病率约为23%，酒精依赖的存在使患抑郁症的风险增加了近5倍。患有抑郁症的患者严重恶化了酒精依赖患者的预后。尽管对预防、治疗和疾病进展有这些巨大的影响，但这种共病背后的机制还不是很清楚。尽管对抑郁症和酒精成瘾涉及的环境和神经生物学因素有很大的了解，但只有少数研究试图将这些经验性的发现转化为更好地理解和治疗合并疾病的患者。此外，成瘾和抑郁的一些神经生物学特征甚至表现出相反的特征。虽然酒精患者的大脑奖励系统的响应性似乎增加了，但抑郁症患者表现出该系统的敏感性降低。虽然抑郁症的特征是默认模式网络连接增加，但酒精成瘾的连接减少被描述为。这项拟议的项目旨在整合之前关于酒精依赖和抑郁相关的奖赏回路和大脑连接的研究，以更好地理解表征它们共病的神经机制。通过不同的实验范式对奖赏和默认模式的网络活动和连通性进行全面的表征，并通过比较抑郁和成瘾患者与共病患者，我们计划确定酒精成瘾和抑郁共病的不同和共同的机制。此外，神经生物学结果将被用来测试一个简短的心理治疗干预计划是否足以对已确定的神经病理机制产生积极影响。

The prevalence of affective disorders in alcohol addiction is estimated to around 23% and the presence of alcohol dependence increases the risk for depression by a factor of almost 5. Suffering from a comorbid depression substantially deteriorates the prognosis of alcohol dependent patients. Despite these tremendous implications for prevention, treatment and disease progression, the mechanisms underlying this comorbidity are not well understood. Although there is significant knowledge of the environmental and neurobiological factors involved in depression and alcohol addiction, only a few studies have tried to translate these empirical findings for a better understanding and treatment of comorbid patients. Furthermore, some of the neurobiological signatures of addiction and depression show even contrary characteristics. While alcohol patients seem to have increased brain reward system responsivity, depressed patients show a reduced sensitivity of the system. While depression is characterized by increased default mode network connectivity, reduced connectivity has been described for alcohol addiction. The proposed project aims to integrate previous research about the reward circuit and brain connectivity associated with alcohol dependence and depression to achieve a better understanding of neural mechanisms characterizing their comorbidity. By means of diverse experimental paradigms allowing a comprehensive characterization of reward and default mode network activity and connectivity and by comparing depressed and addicted patients with comorbid patients, we are planning to identify distinct and common mechanisms underlying the comorbidity of alcohol addiction and depression. In addition, the neurobiological results will be used to test whether a brief psychotherapeutic intervention program is satiable to positively influence the identified neural pathomechanisms.