Processes in the central nervous system are considered to play a major role in the etiology of addiction, and the transition from chronic alcohol consumption to AUD [5]. Therefore, it is of particular interest to examine molecular changes associated with addiction in brain tissue. So far, only few studies have been conducted in postmortem human brain tissue to identify transcriptional changes associated with AUD [6–8]. These studies mainly focused on the prefrontal cortex (PFC) one important part of the neurocircuitry of addiction [9, 10]. The first transcriptome-wide study in the PFC found DE genes implicated in neuronal processes, such as myelination, neurogenesis, and neural diseases, as well as cellular processes, such as cell adhesion and apoptosis [11]. In Brodmann Area 9 downregulation of calcium signaling pathways has been observed in individuals with AUD compared to controls [12]. In the same study, a weighted gene co-expression analysis (WGCNA) pointed towards modules associated with AUD case/control status, which were enriched for nicotine and opioid signaling, as well as immune processes. Another study in the PFC (Brodmann Area 8) showed that co-expression networks associated with lifetime alcohol consumption were enriched for GWAS signals of alcohol dependence [6].
