HR offspring also showed weaker CSD activations (of the sources and sinks) in the frontal and prefrontal regions. Specifically, the lower activations in both P3 amplitude and CSD were found in both younger and older age groups in males but only in younger age groups in females. Neuroimaging studies have found pathophysiological alterations in the brain’s reward system (Diekhof et al., 2008; Park et al., 2010; Tomasi et al., 2010; Muller-Oehring et al., 2013) including altered white matter integrity in individuals with SUD (Bava et al., 2009; Jacobus et al., 2009; McQueeny et al., 2009; Bava et al., 2010), and deficient functional connectivity between frontal lobes and other key structures in subjects who are at high risk for alcoholism (Weiland et al., 2012; Wetherill et al., 2012; Weiland et al., 2013). Forbes et al. (2014) reported that young adults with family history of alcohol dependence exhibited lower medial PFC response. Taken together, all these findings support our hypothesis that suppressed CSD features at the frontal regions during reward processing in the HR group may represent dysfunctional reward circuitry as well as a ‘hypofrontality’, which may mediate or predispose toward risk for developing AUD and/or related disorders in these subjects.
