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Role of astrocytes in thiamine deficiency

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Abstract

Thiamine deficiency (TD) is the underlying cause of Wernicke’s encephalopathy (WE), an acute neurological disorder characterized by structural damage to key periventricular structures in the brain. Increasing evidence suggests these focal histological lesions may be representative of a gliopathy in which astrocyte-related changes are a major feature of the disorder. These changes include a loss of the glutamate transporters GLT-1 and GLAST concomitant with elevated interstitial glutamate levels, lowered brain pH associated with increased lactate production, decreased levels of GFAP, reduction in the levels of glutamine synthetase, swelling, alterations in levels of aquaporin-4, and disruption of the blood–brain barrier. This review focusses on how these manifestations contribute to the pathophysiology of TD and possibly WE.

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Acknowledgments

The senior author (ASH) is a Visiting Professor in the Department of Neurology at Universidade Estadual de Campinas (UNICAMP), Campinas, São Paulo, Brazil. His laboratory at the University of Montreal is supported by the Canadian Institutes of Health Research. S.A. is the recipient of a doctoral scholarship from CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior), Brazil.

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Afadlal, S., Labetoulle, R. & Hazell, A.S. Role of astrocytes in thiamine deficiency. Metab Brain Dis 29, 1061–1068 (2014). https://doi.org/10.1007/s11011-014-9571-y

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