in AUD individuals may be suggestive of neuroadaptation in the hub regions of the reward network, caused by chronic alcohol intake. In general, previous fMRI studies have reported such aberrations in resting state connectivity underlying multiple brain networks in individuals with SUD [19,28,91], including those with AUD [30,31,32,33,63,92,93,94]. Our previous study on the same sample of participants as in the current study reported that AUD individuals manifested altered default mode network (DMN) connectivity compared to controls [63]. It is clear from the findings of our past and current rsFC studies that AUD individuals manifest brain connectivity changes across neural structures involved in spontaneous, self-referential thoughts, as elicited by the DMN [95], as well as the commonly reported reward processing deficits, as elicited by the RN [10]. It is also remarkable to note that both studies showed hypoconnectivity between the ACC and PCC nodes in AUD subjects, confirming the notion of abnormal self-referential processing in these individuals [92]. Furthermore, hypoconnectivity across reward structures during resting state, as found in the current study, may also indicate a vulnerability to relapse in individuals with a history of SUD [96]. Taken together, these findings lend support to the findings of the current study, that
