conditions, it is reasonable to assume that these ‘at risk’ individuals may have difficulty in evaluating the both positive and negative outcomes. Therefore, this finding may indicate blunted monetary outcome salience or deficient neural reward sensitivity in these subjects. This deficient processing could also be due to general “cortical insufficiency”, a concept initially proposed in developmental dyslexia to explain a deficient processing at specific cortical regions (cf. [125]). In addition, similar to alcoholics, who showed weaker CSD activation during reward processing [49], the findings of the present study demonstrate weaker sources and sinks in HR subjects during reward processing in frontal and temporal regions (Fig 5). As shown by the structural and functional MRI studies, it is possible that brain circuitry underlying reward and emotional processing [126–128] as well as the integrity of white matter pathways are altered in individuals with positive family history for alcoholism [129,130]. Pre-existing cognitive deficits in high risk subjects are also evident from the neuropsychological findings showing compromised executive functioning in these subjects [131–133]. Therefore, it is reasonable to assume that asynchronous (delayed) maturation of prefrontal-limbic circuitry may be involved in the predisposition to develop substance use and related disorders in high risk adolescents and
