## 4 Discussion  
We have previously described a relationship, in AUD, between executive deficits and altered connectivity among the fronto-insular-striatal nodes of the \"control\" networks [21]. Here we enriched those data by assessing a core facet of intrinsic brain connectivity such as intra-network coherence, which, compared with other resting-state metrics, represents an earlier biomarker of pathological changes in the intrinsic functional brain architecture [34]. Unlike most previous studies on this topic, we pursued this aim through a multivariate approach to the analysis of both neuro-cognitive and resting-state fMRI data to detect intrinsic networks where altered functional coherence relates to AUD patients' defective performance in cognitive domains transcending single tasks. This approach unveiled a strongly impaired executive domain in AUD patients, with defective performance on TMTa and interference-memory tasks signalling decreased visuomotor speed, attention and working-memory (Supplementary Table S9) [16; 21]. In line with the notion that cognitive impairments in AUD reflect widespread neuro-functional changes involving subcortical nodes [47], the analysis of spectral power revealed decreased intra-network coherent activity, in patients vs. controls, within several components involving the default mode, executive, attentional and striatal brain networks (Figure 1). Such a shift to faster BOLD fluctuations, previously reported in healthy ageing [39], is a typical hallmark of neurological [26] and psychiatric [48; 49; 50] conditions, reflecting the dysregulation of cortical activity and associated cognitive functioning [51]. Since slow fluctuations are considered to underpin temporal synchronicity between regions underlying homologous functions, a decrease of internal coherence might track altered connectivity between and within networks [50] and, accordingly, of neural processes underlying cognitive performance. The present findings therefore contribute to a literature debate reporting either absent [32], selective [30; 31] or widespread [27; 28; 29] alterations of intra-network functional connectivity in AUD. Consistent with the hypothesis that cognitive impairments in AUD reflect more of a global than a selective pattern of brain alteration [47], all of these components also displayed GM atrophy in patients. In keeping with the close relationship between the structural and intrinsic functional brain architecture [52], intra-network temporal coherence could therefore highlight further cues into the brain correlates of defective cognitive performance, and/or compensatory mechanisms, in AUD. We addressed this issue with correlation and interaction analyses, to evaluate quantitative vs. qualitative group differences in the association between intra-network coherent activity and executive performance, respectively. In both groups, higher executive scores were reflected in slower BOLD fluctuations in the anterior salience (16), dorsal attentional (36), and posterior default mode (50) networks (Figure 2A), all supporting cognitive performance proportionally to the level of preservation of their internal coherent activity. While GM concentration was significantly reduced in AUD patients in all of these components, none were associated with a significant decrease of coherence in intrinsic activity, which suggests that its degree reflects individual differences in executive skills along the continuum between normal and impaired performance. This interpretation fits with the role of these networks in driving the interplay between automatic and controlled cognitive processing when salient external stimuli are detected [53]. This switch is indeed prompted by the salience network, including the anterior insula, dorsal anterior cingulate cortex (dACC), basal ganglia and thalamus [54], which activates the attentional and executive control networks to recruit resources for controlled processing [55].