Alcohol Use Disorder (AUD) is a pervasive condition that often presents with marked neurocognitive consequences. From mild executive and memory deficits to severe conditions such as Wernicke–Korsakoff syndrome, cognitive impairment remains one of the most debilitating outcomes of chronic alcohol abuse. Thiamine (vitamin B1) deficiency has long been cited as a critical factor contributing to these deficits, yet recent findings by Teixeira et al. [1] challenge some long-standing assumptions: many patients with AUD display impaired cognition despite having in range blood thiamine levels.
