PGS analysis has been used to evaluate risk for AUD both by others 16 , 75 , 76 and within COGA 77 , 78 , 79 , 80 , 81 , 82 (also see 4. Genetics in this issue). Current COGA studies are now evaluating participants distinguished by extreme high (>90%ile) or low (<10%ile) PGS for AUD, using iPSC‐derived neurons to elucidate possible differences in transcription, neuronal physiology, and response to ethanol. The extensive clinical, neuropsychological, electrophysiological and genetic data available within COGA, in addition to lymphoid cells in the NIAAA/COGA Sharing Repository, can be used for analyses of mechanisms associated with PGS extremes, enabling a multidimensional assessment of AUD risk.
