Chunk #32 — HOW DO NEURAL SIGNATURES ASSOCIATED WITH AUD HELP ELUCIDATE THE ROLE OF BRAIN FUNCTION IN THE RISK AND CONSEQUENCES OF ALCOHOL USE AND AUD ACROSS THE LIFESPAN? — How do genomic factors influence brain functioning across the lifespan and contribute to antecedents and resilience for AUD? — Genome‐wide association studies (GWAS) of neurophysiological phenotypes
COGA conducted the first neural AUD endophenotype GWAS among individuals of African ancestry (AA) and reported genome‐wide significant association between beta EEG power and chromosome 3 variants that influence the expression of BCHE (butyrylcholinesterase 27 ). Several of these variants were also associated with AUD in COGA, and the results replicated in the Yale‐Penn Study of Addiction, an independent sample of AA adults. 27 These variants were also associated with ‘heavy episodic drinking’ among adolescent COGA offspring, 27 suggesting a role of these loci in neural and behavioral disinhibition across different stages of the lifespan. COGA recently conducted the first EEG interhemispheric coherence GWAS, identifying loci in an intergenic region on chromosome 18 that were associated with resting state EEG theta coherence and had both age and sex‐specific effects. These chromosome 18 variants were also associated with higher number of drinks on one occasion and DSM‐5 AUD symptoms in COGA families and associated with alcohol drinker status and alcohol intake frequency in the UK Biobank, an independent sample. 126 These findings provide support for the role of genetic variants on
