Non-coding RNA in alcohol use disorder by affecting synaptic plasticity

Alcohol use disorder (AUD) is one of the most serious public health problems worldwide. AUD is a complex disorder, and there is ample evidence that genetic predisposition is critical to its development. Recent studies have shown that genetic predisposition leads to the onset of AUD, and alcohol metabolism can affect epigenetic inheritance, which in turn affects synaptic plasticity, alters brain function, and leads to more severe addictive behaviors. Non-coding RNAs (ncRNAs), especially microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), play an important role in alcohol addiction. This paper reviews the regulatory role of ncRNAs. ncRNAs are involved in enzyme and neurotransmitter reaction systems during alcohol use disorder. Alcohol consumption regulates the expression of ncRNAs that mediate epigenetic modification and synaptic plasticity, which play an important role in the development of chronic AUD. ncRNAs may be used not only as predictors of therapeutic responses but also as therapeutic targets of AUD. Chronic alcoholism is more likely to lead to neuroimmune disorders, including permanent brain dysfunction. AUD induced by long-term alcoholism greatly alters the expression of genes in the human genome, especially the expression of ncRNAs. Alcohol can cause a series of pathological changes by interfering with gene expression, such as through disordered miRNA-mRNA expression networks, epigenetic modifications, disordered metabolism, and even synaptic remodeling. ncRNAs are involved in the transition from moderate drinking to alcohol dependence.