current study, may have yielded additional information about reward processing deficits in HR offspring; (iv) although the mean trial numbers across the groups in each condition [LR = 42.24 and HR = 40.53 for the gain condition; LR = 39.12 and HR = 36.51 for the loss condition] seems to be sufficient and optimal for the reward-P3 (in view of the findings from earlier studies), further assessments regarding the SNR and minimum/optimal number of trials for component stabilization may have confirmed or improved the validity of current findings; and (v) complex, predictive analytic models, which have not been done in the current study, may be essential to assess the degree to which the factors of genetic risk, substance use, and impulsivity contribute independently as well as relatively contribute to the P3 deficits and CSD profile. Despite these limitations, the study has provided important findings that may have considerable implications for the use of reward related electrophysiological phenotypes to characterize neurocognitive dysfunction in alcoholism and risk status.
