Abstract

Alcoholism is a chronic relapsing brain disorder. Several clinical and preclinical studies indicate that alcohol use disorders (AUD) and anxiety disorders are highly correlated and have a shared etiology, promoting each other’s development and also feeding back into each other’s maintenance. The molecular and epigenetic mechanisms in specific brain circuitry such as the central nucleus of amygdala (CeA) may be involved in the comorbidity of anxiety and alcoholism. Innate or ethanol-induced changes in signaling cascade pathways leading to adaptations at the level of cAMP responsive element–binding (CREB) protein gene-transcription factor function and associated chromatin remodeling due to histone modifications and DNA methylation in the CeA have become one of the emerging mechanisms underlying AUD and anxiety. Studies conducted in the field suggest that histone deacetylases and DNA methyltransferase inhibitors may be potential therapeutic agents to treat or prevent alcoholism with or without comorbid anxiety disorders.

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