A combination of support vector machine and voxel-based morphometry in adult male alcohol use disorder patients with cognitive deficits

Cognitive performance deteriorates with drinking. However, the neural basis of cognitive deficits in alcohol use disorder (AUD) is still incompletely understood. Here we examined the relationship between overall drinking, brain structural alterations and cognitive deficits in AUD. A total of 40 middle-aged AUD males and 40 healthy controls (HC) underwent high-resolution anatomical imaging scans, and the data were analyzed using voxel-based morphometry, support vector machine (SVM) classification and mediation analysis. The AUD patients demonstrated reduced gray matter (GM) volumes that included left amygdala, thalamus, hippocampus, precentral gyrus, cerebellum, calcarine, right supplementary motor area and bilateral superior temporal gyri (voxel-wise p < 0.05, FWE corrected). The SVM results could distinguish AUD from HC with satisfactory classification results (0.8275). GM volumes in the bilateral cerebellum and thalamus, left anterior medial temporal lobe, left nucleus ambiguus + parahippocampus gyrus, left fusiform gyrus, left lingual gyrus, left hippocampus, and right nucleus accumbens had positive correlations with the Montreal Cognitive Assessment (MoCA) scores. Further mediation analysis showed that left cerebellum crus 1 partially mediated the relationship between overall drinking and MoCA scores (standardized beta coefficient = -0.0973, SE = 0.0002, 95% CI = (-0.0006, 0.0000)). Our findings showed widespread GM atrophies and many of these atrophies also mirrored cognitive deficits and were robustly distinguishable. Critically, the left cerebellum crus 1 partially mediated the relationship betweem overall drinking and MoCA scores, suggesting a pathway by which alcohol abuse impairs cognition and accelerates brain ageing in middle-aged AUD males.