Research with animals demonstrates that thiamine deficiency impairs several biochemical pathways requiring the thiamine derivative thiamine pyrophosphate (e.g., transketolase, pyruvate dehydrogenase, and α-ketoacid dehydrogenase) (Thomson et al. 2012), thereby interfering with carbohydrate metabolism (for energy production), lipid metabolism (for production and maintenance of myelin), and amino acid metabolism (for production of glucose-derived neurotransmitters; for example, glutamate and γ-aminobutyric acid [GABA]) (Sechi and Serra 2007; Vetreno et al. 2012). Consequently, the function of essential thiamine-requiring enzymes in the brain (e.g., transketolase, pyruvate dehydrogenase, and α-ketoacid dehydrogenase) is compromised, leading to oxidative stress, cellular energy impairment, and eventually neuronal loss (Thomson et al. 2012).
