Neurobiological markers of vulnerability that exist prior to alcohol initiation have been suggested by neuroimaging, electrophysiological measures, and other neurological findings, (Bauer and Hesselbrock, 1999; Hill et al., 1999; Hill, 2004). Specifically, FHP youth have shown reduced volume of the right orbitofrontal cortex (Hill et al., 2009) and amygdala (Hill et al., 2001); smaller intracranial volume (Gilman et al., 2007); weaker fronto-cerebellar connectivity (Herting et al., 2010); abnormalities in vigilance-related neural activity (Spadoni et al., 2008); and delays in reaching age-appropriate P300 amplitudes (Begleiter et al., 1984; Hill et al., 1999; Polich et al., 1994) and postural control (Hill et al., 2000). Several of these neurobiological differences have suggested abnormalities in frontoparietal circuitry (Hada et al., 2001; Rangaswamy et al., 2004; Spadoni et al., 2008), including the posterior parietal cortex (PPC) and dorsolateral prefrontal cortex (DLPFC), as these areas are involved in inhibitory control, executive control, and decision-making (Lundqvist, 2010). As such, abnormalities in frontoparietal connectivity may contribute to the neurocogntive abnormalities observed among FHP youth and may be a premorbid neurobiological marker for the development of AUDs.
