in some locations and frequency bands (Supplemental Figure S5). These developmental changes may reflect increasing white matter known to occur in the early 20s [68]. From data observed in other developmental studies [69] measured at shorter time intervals than those in the current study, it is likely that individuals change more rapidly than what can be observed by mean trajectories over brief time intervals, i.e., there are growth spurts in an individual’s neural development. Thus, developmental differences in the influence of AD PRS on EEG coherence observed in this study may reflect genetic influences on coherence growth spurts. Results from this study show that connectivity differences associated with PRS predate significant alcohol use, and sensitivity analyses did not detect a significant effect of drinking (maximum number of drinks consumed in a typical week, last 12 months) or DSM-5 AUD (lifetime diagnosis) on the PRS-EEG coherence association (Supplementary Tables S5 and S6). This suggests that the connectivity differences observed in this study are likely markers of risk, rather than a consequence of heavy alcohol use. Interestingly, the influence of PRS on EEG connectivity differed among those with and without AUD (lifetime diagnosis), suggesting that the PRS has a greater influence on
