Familial AUD has been linked to unique patterns of neuroanatomy (10, 11), neurocognition (12, 13), neurophysiology (14), and brain functioning (15). As some these neural markers are no longer detectable in FHP adults, such patterns have been theorized to be evidence of an inherited neurodevelopmental lag in FHP youth (16). For example, since amygdala and intracranial volume increase over childhood and adolescence, reduced volumes in FHP youth may indicate a developmental lag (12, 13). Also, the P300 component of the event-related potential has shown reduced amplitude in FHP children and adults (16) as well as in heavy drinkers (17), suggesting a potential endophenotype of alcoholism (18). This feature is most consistently displayed in FHP individuals under age 18, after which FHP individuals begin to resemble FHN peers, suggesting an inherited developmental lag (16). Finally, delayed maturation of postural sway (19) has also been implicated in FHP youth. These neural features, which appear to be more salient in youth, may confer greater risk for the development of future AUD.
