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Benefits of Thiamin (Vitamin B1) Administration in Neurodegenerative Diseases may be Due to Both the Coenzyme and Non-coenzyme Roles of Thiamin
Victoria I Bunik*
Belozersky Institute of Physicochemical Biology and Faculty of Bioengineering and Bioinformatics of Lomonosov Moscow State University, 119992 Moscow, Russian Federation
- Corresponding Author:
- Victoria I. Bunik
Belozersky Institute of Physicochemical Biology and Faculty of Bioengineering and Bioinformatics of Lomonosov Moscow State University, Vorob’evy Gory 1, 119992 Moscow, Russian Federation
Tel: +7-495-939-4484
E-mail: bunik@belozersky.msu.ru
Received date: November 20, 2014; Accepted date: December 11, 2014; Published date: December 18, 2014
Citation: Bunik VI (2014) Benefits of Thiamin (Vitamin B1) Administration in Neurodegenerative Diseases may be Due to Both the Coenzyme and Non-coenzyme Roles of Thiamin. J Alzheimers Dis Parkinsonism 4:173. doi:10.4172/2161-0460.1000173
Copyright: © 2014 Bunik VI. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Although no systematic studies on therapeutic value of thiamin administration in neurodegenerative diseases are available to draw statistically significant conclusion, beneficial effects of thiamin in the diseases have been observed in independent case reports. The data are usually interpreted as improvement of central metabolism due to the coenzyme role of thiamin diphosphate (ThDP) in the transketolase, pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase reactions. However, several lines of evidence support a view that the thiamin action is not limited to this mechanism. First, no firm correlation between the benefits of thiamin administration and levels of ThDP and/or ThDP-dependent enzymes in brain has been shown. Second, synthesis of non-coenzyme derivatives of thiamin, such as thiamin triphosphate and its adenylated form, occurs in nature from bacteria to mammals. Third, emerging data suggest significance of the non-coenzyme derivatives of thiamin for cellular responses to metabolic stress and DNA damage. The review draws attention to importance of these new data for interpreting molecular mechanisms of the consequences of thiamine deficiency or supplementation.
