We report the robust associations of polygenic risk for SCZ with developmental trajectories of neural connectivity among unaffected individuals: in particular, we observed that males with higher polygenic risk for SCZ exhibit increased EEG coherence in the alpha frequency band in posterior brain regions between the ages of 15 and 19. Although the “disconnection hypothesis”18 has been one of the main etiological models of SCZ for decades and has been generally supported46, empirical evidence has been somewhat mixed, pointing to more complex abnormalities in the connectivity pattern including both increases and decreases of connectivity depending on specific location, subjects’ state (e.g., during a task vs. in the resting-state), and neuroimaging modality47–49. Findings from our study of increased connectivity correspond well to previous work demonstrating higher resting-state alpha EEG coherence both within and across hemispheres among individuals with SCZ and in their relatives5. While increased connectivity observed among individuals with higher SCZ PRS may seem counterintuitive to many dysconnectivity hypotheses in psychotic illness, several previous studies have found similar patterns of increased connectivity among those with SCZ and their relatives5,50–54. For
