HV deficits milder than that of WKS have been observed in uncomplicated AUD compared to healthy controls (Pitel et al., 2012b), which are attributed to loss of WM and decreased axonal diameter (Harding et al., 1997), glial cell loss (Korbo, 1999), or reduced incorporation of newly formed neurons to the dentate gyrus (He et al., 2005). The hippocampus plays a central role in the formation, consolidation, and retention of recent (or declarative) memories (Burgess et al., 2002, Tamnes et al., 2014). Memory impairments have been observed in early abstinent AUD individuals (e.g., Kopera et al., 2012) and various mechanisms implicating hippocampus have been proposed (Chanraud et al., 2009, Zahr et al., 2017). Therefore, these results also provide a neuroanatomical substrate for memory impairments in AUD.
