These data should be considered in light of possible limitations. Our relatively small sample size may have precluded detection of white matter anisotropy or diffusivity differences. Similarly, our a priori decision to limit analyses to the specified seed regions and selected white matter tracts to minimize Type I error may have increased Type II error, resulting in unidentified differences between groups. We also acknowledge that effect sizes are modest and may be related to sample characteristics, such as moderate density of familial alcohol use disorder density among FHP youth. Since analyses were not longitudinal, we cannot ascertain whether differences in frontoparietal connectivity predicts alcohol use in FHP youth. Future studies will need to examine whether abnormalities in frontoparietal connectivity directly predicts alcohol use disorders. This study is strengthened; however, by examining functional connectivity and white matter microstructure in well-matched, substance-naïve youth, and we were therefore able to rule out several potential confounds. Furthermore, we combined fcMRI and DTI methodologies to not only examine neural regions implicated in the development of AUDs but how they are functionally integrated.
