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Chunk #0 — Introduction

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Integrated single-cell multiomic profiling of caudate nucleus suggests key mechanisms in alcohol use disorder.
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Excessive alcohol use creates many serious physical, emotional, and social problems and is responsible for about 3 million deaths worldwide each year1. Alcohol use disorder (AUD) is a serious and common psychiatric disorder that is characterized by excessive alcohol consumption and consequent psychological and interpersonal problems stemming from preoccupation with and a loss of control over drinking2. The risk of developing AUD depends on both genetic and environmental factors; between 50% and 60% of the difference in vulnerability to AUD is inherited3. While recent large-scale genome-wide association studies (GWAS) have identified hundreds of loci associated with alcohol consumption4,5 and AUD6–8, it is not yet clear which genes within the loci are responsible, nor how they contribute to AUD.