Coppens Violette, Morrens Manuel, Destoop Marianne, Dom Geert
Faculty of Medicine and Health Sciences, Collaborative Antwerp Psychiatric Research Institute (CAPRI), University of Antwerp, Antwerp, Belgium.
Scientific Initiative of Neuropsychiatric and Psychopharmacological Studies (SINAPS), University Department of Psychiatry, Duffel, Belgium.
Front Psychiatry. 2019 Sep 12;10:632. doi: 10.3389/fpsyt.2019.00632. eCollection 2019.
Of late, evidence emerges that the pathophysiology of psychiatric diseases and their affiliated symptomatologies are at least partly contributable to inflammatory processes. Also in alcohol use disorders (AUD), this interaction is strongly apparent, with severely immunogenic liver cirrhosis being one of the most critical sequelae of chronic abusive drinking. This somatic immune system activation negatively impacts brain functioning, and additionally, alcohol abuse appears to have a direct detrimental effect on the brain by actively stimulating its immune cells and responses. As cognitive decline majorly contributes to AUD's debility, it is important to know to what extent impairment of cognitive functioning is due to these (neuro-)inflammatory aberrations. We hereby summarize the current existing literature on the interplay between AUD, inflammation, and cognition in a systematic review according to the PRISMA-P guidelines for the systematic review. Although literature on the role of inflammation in alcohol use-related cognitive deficiency remains scarce, current findings indicate that pro-inflammatory processes indeed result in exacerbation of several domains of cognitive deterioration. Interestingly, microglia, the immune cells of the brain, appear to exert initial compensatory neuroprotective functionalities upon acute ethanol exposure while chronic alcohol intake seems to attenuate these responses and overall microglial activity. As these results indicate inflammation to be of importance in cognitive impairment following alcohol consumption and might as such provide alternate therapeutic avenues, a considerable increase in research efforts in this domain is urgently required.
最近，有证据表明精神疾病的病理生理学及其相关症状至少部分归因于炎症过程。在酒精使用障碍（AUD）中，这种相互作用也非常明显，严重的免疫原性肝硬化是长期酗酒最关键的后遗症之一。这种躯体免疫系统的激活对大脑功能产生负面影响，此外，酒精滥用似乎通过积极刺激大脑的免疫细胞和反应，对大脑产生直接的有害影响。由于认知能力下降是导致AUD患者虚弱的主要原因，了解认知功能损害在多大程度上是由这些（神经）炎症异常引起的非常重要。我们在此根据系统评价的PRISMA - P指南，对目前关于AUD、炎症和认知之间相互作用的现有文献进行系统综述。尽管关于炎症在酒精使用相关认知缺陷中的作用的文献仍然很少，但目前的研究结果表明，促炎过程确实会导致认知衰退的几个领域恶化。有趣的是，大脑的免疫细胞小胶质细胞在急性乙醇暴露时似乎会发挥初始的代偿性神经保护功能，而长期饮酒似乎会减弱这些反应以及整体小胶质细胞的活性。由于这些结果表明炎症在饮酒后认知障碍中具有重要作用，因此可能提供替代治疗途径，迫切需要在该领域加大研究力度。
