Several limitations apply to our study. First, we cannot distinguish between effects being a consequence of chronic alcohol consumption or addiction. Second, although we corrected for PMI, which can influence tissue quality as a confounding factor, it cannot be ruled out that other characteristics not easily accounted for, such as cause of death, or blood alcohol level for which the majority of individuals have missing data, influenced gene expression. Third, although the sample size is comparatively large for postmortem brain studies in the addiction field, the small number of differentially expressed genes is likely attributable to limited power. Lastly, analyzing bulk tissue does not adequately reflect the diversity of cell types across different brain regions and future studies on the single-cell level are needed to investigate cell-type-specific transcriptional changes associated with AUD.
