and DTI measures with functional association findings (Colrain et al., 2011, Pfefferbaum et al., 2000, Pitel et al., 2012a). Additionally, combined structural results and relative contributions of different GM and WM regions in explaining shared variance with performance on neuropsychological tests suggest abnormalities in brain circuits, rather than distinct brain regions, as responsible for the observed functional deficits. Zahr et al. (2017) have recently identified three independent and non-overlapping frontally-based networks (fronto-fugal), involving coordinated activities of several regions interacting with frontal structures rather than a single area in prefrontal cortices, that mediate specific neuropsychological deficits in AUD. These authors propose that abnormalities of brain structure and function are due to AUD and not merely aging. More refined knowledge of compromised and spared structures and functions in AUD would help in determining mediational effects that could enhance therapeutic efforts to redirect neural recruitment from the usual but disrupted paths and networks to functional alternatives, possibly through behavioral therapy (Zahr et al., 2017). Future studies should investigate the relationship of structural characteristics and connectivity with functional connectivity, combining data from different techniques such as diffusion tractography with functional connectivity measures, including resting-state and event-related functional networks, in order to understand the link
