Cellular nature of major depressive disorder and alcohol use disorder comorbidity: An overview

Abstract

The co-occurrence of alcohol use disorders and depression is increasing in our society due to their wide prevalence. Both alcohol use disorders (AUD) and depression increase susceptibility to disability and mortality, and their symptoms are closely linked to the brains reward circuits. While the pathogenesis of AUD and depression is well-researched, the mechanism of comorbidities remains a challenge. Individuals with depression may use alcohol for self-medication, leading to the formation of AUD over time. Abrupt cessation of alcohol consumption in individuals with long-term AUD can result in neurotransmitter abnormalities and an elevated risk of depression or relapse. This review primarily focuses on basic research and summarizes neurotransmitters such as GABA, glutamate, dopamine, norepinephrine, and 5-HT in relation to Major Depressive Disorder and AUD. Currently, the effectiveness of treatment for comorbidities is not clearly evident. Our goal is to comprehensively explore the cellular attributes associated with these comorbidities in order to identify new avenues for therapeutic interventions.