The predominant pattern observed in AUD individuals was hypoconnectivity (9 out of 12 connections) across subcortical reward regions (5 connections) followed by cortical (3 connections) and cortical–subcortical (1 connection) subnetworks. Specifically, these hypoconnected nodes include key reward regions such as the VTA, amygdala, hippocampus, thalamus, pallidum, putamen, insula, ACC, PCC, and OFC, possibly indicating lower or less efficient neural communication across these subnetworks [6]. Since addiction has been characterized as a reward deficiency syndrome [97], hypoconnectivity across these reward structures in abstinent AUD subjects may indicate reduced responsiveness to rewarding stimuli during resting state, possibly due to decreased dopamine function in these individuals [50,98]. Although elevated levels of dopamine in the dorsal striatum are associated with motivation to seek and consume alcohol and drugs, long-term substance use is associated with decreased dopaminergic function, as evidenced by reductions in D2 dopamine receptors and dopamine release in the striatum in addicted subjects [50], which can also lead to reduced activity in other cortical reward regions such as the orbitofrontal cortex and cingulate gyrus, resulting in loss of control and compulsive substance use.
