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Global changes in gene expression and splicing in alcoholic liver disease
Abstract Alcohol use disorder is a widespread illness commonly leading to alcoholic liver disease (ALD) and cirrhosis with an increased incidence of hepatocellular carcinoma (HCC), but the mechanisms of alcohol-related oncogenesis in the liver are incompletely understood. We tested the hypothesis that ALD predisposes to HCC via dysregulation of splicing.
Leptin Gene and Leptin Receptor Gene Polymorphisms in Alcohol Use Disorder: Findings Related to Psychopathology
Introduction Alcohol use disorder (AUD) is highly prevalent in the U.S., affecting ~14.1 million adults (1). It is frequently co-morbid with other addictive and psychiatric disorders, and there is substantial evidence suggesting a bidirectional relationship between AUD and other psychopathologies (2).
A molecular mechanism for choosing alcohol over an alternative reward
“Only” about 10 to 15% of people exposed to alcohol develop alcohol-related problems. The behavioral repertoire of people confronted with opportunities to consume alcohol involves numerous choices between this drug reward and healthy alternatives. Augier et al. established a choice procedure that begins to address alcohol addiction in rats (see the Perspective by Spanagel).
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