Alcohol use disorder (AUD) is a chronic relapsing disorder characterized by an impulsive drive toward continued alcohol consumption despite negative consequences [1,2,3]. Individuals with AUD manifest a variety of structural and functional brain abnormalities [4,5,6,7]. For example, numerous functional magnetic resonance imaging (fMRI) studies in AUD have shown region-specific deficits in brain activation, mainly implicating the frontal lobes [8,9], during cognitive and affective processing, involving inhibitory control, executive functioning, memory, and reward processing [10,11]. These functional abnormalities during cognitive processing in AUD have been well-characterized by neurophysiological studies of electroencephalogram (EEG), event-related potentials/oscillations (ERP/ERO) [5,6,12], as well as by neuropsychological studies [7,13] and behavioral manifestations, such as impulsivity [14]. Structural MRI studies using diffusion tensor imaging (DTI) have shown abnormalities in whiter matter integrity and connectivity across several fiber tracts connecting different brain regions across cortical as well as subcortical structures, due to chronic alcohol exposure [4,15,16,17]. Recent studies have identified that neurostructural damage in AUD was significantly related to functional deficits in executive performance, which was in turn associated with microstructural changes in large-scale brain networks [18,19]. In summarizing
