标题：Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy
作者：Liu, Dexiang; Ke, Zunji; Luo, Jia
作者机构：[Liu, Dexiang] Shandong Univ, Sch Med, Dept Med Psychol, 44 Wenhua Xi Rd, Jinan 250012, Shandong, Peoples R China.; [Liu, Dexiang; Luo, Jia] Univ Ke 更多
通讯作者：Luo, J;Luo, J
通讯作者地址：[Luo, J]Univ Kentucky, Dept Pharmacol & Nutr Sci, Coll Med, 132 Hlth Sci Res Bldg,1095 Vet Dr, Lexington, KY 40536 USA;[Luo, J]Shanghai Univ Tradit Ch 更多
关键词：Alcoholism; Protein degradation; Reactive oxygen species; Unfolded; protein response; Vitamin B1
摘要：Thiamine (vitamin B1) is an essential nutrient and indispensable for normal growth and development of the organism due to its multilateral participation in key biochemical and physiological processes. Humans must obtain thiamine from their diet since it is synthesized only in bacteria, fungi, and plants. Thiamine deficiency (TD) can result from inadequate intake, increased requirement, excessive deletion, and chronic alcohol consumption. TD affects multiple organ systems, including the cardiovascular, muscular, gastrointestinal, and central and peripheral nervous systems. In the brain, TD causes a cascade of events including mild impairment of oxidative metabolism, neuroinflammation, and neurodegeneration, which are commonly observed in neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD). Thiamine metabolites may serve as promising biomarkers for neurodegenerative diseases, and thiamine supplementations exhibit therapeutic potential for patients of some neurodegenerative diseases. Experimental TD has been used to model aging-related neurodegenerative diseases. However, to date, the cellular and molecular mechanisms underlying TD-induced neurodegeneration are not clear. Recent research evidence indicates that TD causes oxidative stress, endoplasmic reticulum (ER) stress, and autophagy in the brain, which are known to contribute to the pathogenesis of various neurodegenerative diseases. In this review, we discuss the role of oxidative stress, ER stress, and autophagy in TD-mediated neurodegeneration. We propose that it is the interplay of oxidative stress, ER stress, and autophagy that contributes to TD-mediated neurodegeneration.