Abstract
An acute deficiency of thiamin in animals generally leads to focal brain lesions characterized by necrosis and petechial hemorrhage in particular brain regions. In humans, a clinical syndrome based on the brain damage induced by thiamin deficiency is known as Wernicke-Korsakoff syndrome (WKS). To examine the pathogenesis of WKS, rodent models for WKS have been developed and extensively studied. However, the precise mechanism by which thiamin deficiency produces necrotic lesions in particular brain regions is still unclear. In this review, we describe a history of the research on WKS, neuropathological changes induced by thiamin deficiency, and recent advances in understanding the pathogenesis of experimental WKS in the rodent models. Based on the experimental data in the recent literatures, we discuss possible pathways from thiamin deficiency to neuronal death.
