Background: Alcohol dependence is one of the leading contributors to the burden of disease in the world. A range of genetic and environmental risk factors has been identified to date, and preclinical and clinical studies including imaging studies have identified neuronal networks involved in the development of alcohol dependence. Methods: We review genetic and environmental risk factors for the development of alcohol addiction as well as structural and neuronal changes, including their transmitter systems, due to regular alcohol intake. Results: Stress as well as family background and, in juveniles, the peer group could be identified as environmental risk factors for alcohol dependence. Heritability is estimated at around 50%, and it seems to be comparable in women and men. There is ongoing research on a broad range of putative endophenotypes such as tolerance of the effects of alcohol intake or personal traits like ‘impulsivity'. On the neurobiological level, chronic alcohol intake seems to render mesolimbic circuits hypersensitive to alcohol and alter the motivational reward system including dopaminergic neurotransmission. Conclusion: Environmental and genetic risk factors, and especially their interaction, facilitate the development of alcohol dependence. Ongoing alcohol intake results in profound alterations of neuronal systems crucial for motivation, learning, memory and cognition control. Future studies should further combine the knowledge of neurobiological mechanisms and risk factors to develop new prevention strategies.

No abstract