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Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy

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Abstract

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.

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Abbreviations

AD:

Alzheimer’s disease

ALS:

Amyotrophic lateral sclerosis

ATF6:

Activating transcription factor-6

ER:

Endoplasmic reticulum

HD:

Huntington’s disease

HNE:

4-Hydroxynonenal

IRE1:

Inositol requiring protein-1

KGDHC:

α-Ketoglutarate dehydrogenase complex

PD:

Parkinson’s disease

PDHC:

Pyruvate dehydrogenase complex

PERK:

Protein kinase RNA-like ER kinase

PRD:

Prion-related diseases

ROS:

Reactive oxygen species

TD:

Thiamine deficiency

TPP:

Thiamine pyrophosphate

UPR:

Unfolded protein response

WKS:

Wernicke-Korsakoff syndrome

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Acknowledgments

We thank Jacqueline Frank for reading this manuscript. This work was supported by grants from the National Institutes of Health (NIH) (AA017226 and AA015407). It is also supported in part by the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development (Biomedical Laboratory Research and Development BX001721).

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Authors and Affiliations

  1. Department of Medical Psychology, Shandong University School of Medicine, #44 Wenhua Xi Road, Jinan, Shandong, 250012, People’s Republic of China

    Dexiang Liu

  2. Department of Pharmacology and Nutritional Sciences, College of Medicine, University of Kentucky, 132 Health Sciences Research Building, 1095 Veterans Drive, Lexington, KY, 40536, USA

    Dexiang Liu & Jia Luo

  3. Department of Biochemistry, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China

    Zunji Ke & Jia Luo

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  1. Dexiang Liu
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Correspondence to Jia Luo.

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Liu, D., Ke, Z. & Luo, J. Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy. Mol Neurobiol 54, 5440–5448 (2017). https://doi.org/10.1007/s12035-016-0079-9

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