possible that alcohol-induced reduction of myelin may be caused by inflammatory or epigenetic processes [8, 80]. In addition, a reduction of axonal fibers may have occurred due to direct alcohol toxicity to neuronal and glial cells. Lastly, changes in the chemical composition of fibers, as well as the ratio between axonal fibers, oligodendrocytes, and other glial cells in AUD patients, may account for observed effects (e.g., [12, 80] for review). Together, chronic high alcohol consumption has been shown to cause multiple molecular and systemic changes that may account for observed WM alterations. In this regard, it is interesting to note structural damages observed in AUD patients partially regenerated during prolonged abstinence [63]. Alternatively or in addition, a preexisting state of WM alterations may also be the cause or at least facilitate the development of AUD, for example in individuals with a family history of AUD [81]. Furthermore, it should be considered that the largest cluster of the main analysis and the second-largest cluster of the DTI sub-analysis cover the fornix. The fornix is a thin structure located close to the ventricles, which makes it particularly susceptible to partial volume effects [82]. This effect occurs when in a voxel the signal
