Alcohol use disorder (AUD) results from a complex interaction of genetic and environmental liabilities across the lifespan [1]. Variations in brain structure and function are both antecedents to AUD and consequences of the effects of excessive alcohol consumption [2]. Differences in the connectivity of large-scale brain networks are observed among individuals with neuropsychiatric disorders, including AUD, and in their offspring [3]. Given its exquisite temporal resolution (millisecond range), EEG coherence has proven to be a useful measure of neural connectivity patterns in specific EEG frequency bands which, alongside clinical and fMRI data with spatial resolution allowing for anatomical specificity, can further our understanding of neural mechanisms of AUD [4]. Research characterizing genetic variation for AUD with respect to measures of neural connectivity can advance understanding of how genomic risk for AUD affects neurocognitive function.
