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The impact of oxidative stress in thiamine deficiency: A multifactorial targeting issue
Authors:Alan S. Hazell  Samantha Faim  Guilherme Wertheimer  Vinicius R. Silva  Cleiton S. Marques
Affiliation:1. Department of Medicine, University of Montreal, Montreal, Quebec, Canada;2. Departamento de Neurologia, Universidade Estadual de Campinas (UNICAMP), Campinas, São Paulo, Brazil
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.
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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