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 thiamine deficiency on the brain and can be used to determine susceptible brain regions as a function of time of insult (Dror et al. 2010; Zahr et al. 2014a) as well as relationships between neuroinflammatory markers and brain insult (Zahr et al. 2014a). Such studies have also been used to confirm a mechanism of toxicity suspected based on research in humans (e.g., Harper 1980; Koguchi et al. 2004; Navarro et al. 2008): that glucose loading in a thiamine-deficient state can precipitate WE (Jordan et al. 1998; Zahr et al. 2014a), likely involving a breakdown of the blood–brain barrier (Nixon et al. 2008; Zelaya et al. 1995). In animals, postmortem followup can be used to confirm and extend in vivo findings. For example, electron microscopy showed a higher percentage of small fibers and myelin thinning in the corpus callosa of thiamine-deficient animals relative to controls (He et al. 2007).
