Bizarre Research on Wernicke's Encephalopathy

I'm looking through some of these articles (and a book on google books: http://books.google.com/books?lr=&q=%22thiamine+turnover%22+Parvez) on Wernicke's encephalopathy and experimental models of thiamine deficiency in the central nervous system, in animals, and the research is just crazy. There is a good section in that book, in which the authors discuss thiamine turnover in the brain. The authors say that the brain has a limited amount of superfluous thiamine, limited stores. I think ethanol must increase thiamine turnover, but there probably are articles on it somewhere. But the research on Wernicke's encephalopathy is just crazy. I was reading a review article on it, and it's just like one article finds one thing and another finds some bizarrely-different thing. The authors of that book cite articles, on page 298, saying that there's no ATP depletion in CNS thiamine deficiency? Come on...There's all this cerebral edema and degeneration, and it's all occurring without ATP depletion, apparently. Give me a break. I mean, it's humorous in some ways, but the research is really all over the ballpark.

One fairly consistent finding to come out of the research is that transketolase activity (a thiamine diphosphate-dependent enzyme) is less affected in Wernicke's encephalopathy or experimental, CNS thiamine depletion in rodents, and the activity of the alpha-ketoglutarate dehydrogenase (KGDH) complex (also dependent on thiamine-derived cofactors) is apparently reduced more than the activities of the other enzyme complexes (the branched-chain alpha-keto acid dehydrogenase and pyruvate dehydrogenase complexes, the other thiamine-dependent enzyme systems) are. The KGDH complex is rate-limiting for the utilization of glucose in the brain, and thiamine deficiency is going to produce no reduction in ATP synthesis or in ATP levels? I know this is not that hot an area of research anymore, but it's still interesting.