The impact of oxidative stress in thiamine deficiency: A multifactorial targeting issue |
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Authors: | Alan S. Hazell Samantha Faim Guilherme Wertheimer Vinicius R. Silva Cleiton S. Marques |
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Affiliation: | 1. Department of Medicine, University of Montreal, Montreal, Quebec, Canada;2. Departamento de Neurologia, Universidade Estadual de Campinas (UNICAMP), Campinas, São Paulo, Brazil |
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Abstract: | Thiamine (vitamin B1) deficiency, the underlying cause of Wernicke–Korsakoff syndrome, is associated with the development of focal neuronal loss in vulnerable areas of the brain. Although the actual mechanism(s) that lead to the selective histological lesions characteristic of this disorder remain unresolved, oxidative stress has been shown to play a major role in its pathophysiology. In this review, the multifactorial influence of oxidative stress on a variety of processes known to take part in the development of structural lesions in TD including excitotoxicity, neuroinflammation, blood–brain barrier integrity, mitochondrial integrity, apoptosis, nucleic acid function, and neural stem cells will be discussed, and therapeutic strategies undertaken for treating neurodegeneration examined which may have an impact on the future treatment of this important vitamin deficiency. |
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Keywords: | AD, Alzheimer&rsquo s disease ATP, adenosine triphosphate BBB, blood&ndash brain barrier eNOS, endothelial nitric oxide synthase GFAP, glial fibrillary acidic protein GLT-1, glutamate transporter 1 GLAST, glutamate/aspartate transporter KGDHC, α-ketoglutarate dehydrogenase complex MAO, monoamine oxidase NMDA, N-methyl-d-aspartate PD, Parkinson&rsquo s disease ROS, reactive oxygen species SINDEPAR, Sinemet-Deprenyl-Parlodel TCA, tricarboxylic acid cycle TD, thiamine deficiency TSPO, translocator protein (18 kDa) WKS, Wernicke&ndash Korsakoff syndrome |
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