There are two experimental approaches to model WE in rodents. The slower approach uses a thiamine-deficient diet (i.e., feeding with a thiamine-deficient chow), which can take 3–4 weeks to produce symptoms. Behavioral symptoms can be achieved in ~2 weeks using a combination of a thiamine-deficient chow and intraperitoneal (i.p.) administration of a thiamine pyrophosphokinase inhibitor such as pyrithiamine (Hazell and Butterworth 2009). Both models result in symptoms that mimic those observed in humans with WE (Pitkin and Savage 2001). Structural MRI findings in thiamine-deficient animals show similar patterns of brain changes, including hyperintense signals observed on T2-weighted images in thalamus, collicular bodies (Dror et al. 2010; Jordan et al. 1998; Pfefferbaum et al. 2007; Zahr et al. 2014a), hypothalamus, hippocampus (Jordan et al. 1998), mammillary bodies (Pfefferbaum et al. 2007), corpus callosum, and superior cerebellar peduncles (Dror et al. 2010). Thiamine deficiency may cause degeneration through neuroinflammatory mechanisms (Abbott 2000; Hazell and Butterworth 2009). In rats, inflammatory genes were highly expressed in vulnerable brain regions (Vemuganti et al. 2006). MRI in animal models permits further probing of the effects of
