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Thiamine is essential for brain function. Thiamine deficiency (TD) causes severe damage to the central nervous system. TD-induced neuronal damage shares many features of neurodegenerative diseases associated with aging. Thiamine deficiency in animals has been used to model and study neurodegeneration and its underlying cellular/molecular mechanisms. Disruption of intracellular calcium ([Ca2+]i,) homeostasis has been implicated in aging associated neurodegeneration. Current evidence indicates that thiamine deficiency induces Ca2+ influx and causes Ca2+ overload. TD-induced Ca2+ influx is mediated by a glutamate receptor, GluR2. TD-mediated disruption of [Ca2+]i, may underlie glutamate excitotoxicity or endoplasmic reticulum (ER) stress-induced neurodegeneration in selective brain structures.

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