Developmental criminological research findings, such as the influential developmental taxonomy theory by Moffitt [51, 52], have suggested the existence of distinctive offending patterns across the life-course [53]. These developmental trajectories of ASB are thought to have different underlying etiological processes, with relatively more variance explained by genetic factors for life-course-persistent offending as compared to the more socially influenced adolescence-limited offending. Barnes et al. have previously produced evidence that heritability estimates were not uniform across different offending groups, suggesting that the causal processes may vary across offending patterns [54, 55]. In the present study we found a trend of higher PRS for ASB showing a stronger association with the life-course-persistent trajectory of ASB as compared to the low ASB group. The life-course-persistent trajectory is also known to be associated with profound brain alterations and diminished neurological health [56]. These findings are important since they have the capacity to help improve the current understanding of downstream neurobiological mechanisms relevant to the etiology of antisocial development [56]. Sufficiently powered future studies should thus aim to further elucidate the genetic risk and protective factors that underlie different offending trajectories [57].
