older individuals, some studies have also demonstrated early developmental changes in brain structures and function that varied by APOEε4 status (Iacono & Feltis, 2019), with healthy young ε4 carriers (age 3–20) displaying smaller hippocampi, larger medial orbitofrontal cortical areas, and lower scores on executive function, working memory, and attention tasks (Chang et al., 2016). These neurobiological features associated with young carriers of APOEε4 may contribute to an increased vulnerability to PTSD, as well as to AUD, where the interaction between genetics and environmental stressors can lead to maladaptive coping mechanisms involving heavy alcohol use (Averill et al., 2019; Bremner, 2006). Most studies investigating the impact of PTSD on the relationship between APOEε4, and neurocognitive outcomes have focused on older adults with less attention paid to the way trauma exposure and APOEε4 may contribute to differences in cognitive functioning observed in adolescence and young adulthood. Accordingly, while we know that differences in cognition related to PTSD, alcohol use, and APOEε4 have been detected in adolescence and young adulthood, we do not yet know the degree to which these influential risk factors may converge to influence brain functioning during this critical developmental period jointly. Therefore, there is a need to better understand
