Additionally, the nucleotide sequence of the transketolase coding region in fibroblasts derived from two Wernicke-Korsakoff (WK) patients was compared to that of two nonalcoholic controls.
After a series of investigations published by several authors little evidence remains to support the hypothesis of an inborn transketolase abnormality in Wernicke-Korsakoff patients.
Selective increase of neuronal cyclooxygenase-2 (COX-2) expression in vulnerable brain regions of rats with experimental Wernicke's encephalopathy: effect of nimesulide.
The most significant identified brain regions were the Prefrontal Cortex (linked to stimulus driven executive control), Wernicke's area (linked to Phonological code retrieval), the right IFG, and Broca's area (linked to syllabification).
Our findings suggest that treatment with fedratinib does not lead to or alter the progress of TD, and do not support the notion that administration of this JAK-2 inhibitor directly results in the development of WE due to inhibition of thiamine transport.
Homozygous or compound heterozygous mutations in SLC19A3 cause two distinct clinical phenotypes, biotin-responsive basal ganglia disease and Wernicke's-like encephalopathy.