In recent years, clinical addiction researchers have forged new paths. Motivated by dimensional models of addiction that reframe disordered drug use as arising from multiple processes in distinct functional domains [1], these novel approaches characterize several neurobehavioral mechanisms in the same individuals and their interactive influence on drug use. This innovative perspective integrates neuroscience findings and the vast heterogeneity in substance use phenotypes to devise more effective strategies to target treatments and interventions. Moreover, it emphasizes a need to understand the complex and varied pathways to addiction.

The report by Joyner et al. in this issue of Neuropsychopharmacology is an important contribution to the burgeoning literature in this area [2]. Notably, the findings inform a heterogeneous etiology of disordered drinking and the interplay of genetic and external factors. The authors analyzed electroencephalography (EEG) data and self-reports to determine how cognitive disinhibition (executive control domain) and alcohol cue reactivity (ACR, incentive salience domain) relate to problematic alcohol involvement (PAI) in emerging adults with past-year binge drinking but no current or previous history of alcohol use disorder (AUD). Neurophysiological data comprised event-related potential (ERP) P3 amplitudes elicited by oddball stimuli in separate visual tasks. In the rotating heads task, low amplitude Target-P3 reflected high disinhibition, whereas high amplitude ACR-P3 reflected greater alcohol cue reactivity in the picture viewing task.

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