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dc.contributor.authorAllaman, Igor
dc.contributor.authorBélanger, Mireille
dc.contributor.authorMagistretti, Pierre J.
dc.date.accessioned2015-02-10T07:57:52Z
dc.date.available2015-02-10T07:57:52Z
dc.date.issued2015-02-09
dc.identifier.citationAllaman I, Bélanger M and Magistretti PJ (2015) Methylglyoxal, the dark side of glycolysis. Front. Neurosci. 9:23. doi: 10.3389/fnins.2015.00023
dc.identifier.issn1662-453X
dc.identifier.pmid25709564
dc.identifier.doi10.3389/fnins.2015.00023
dc.identifier.urihttp://hdl.handle.net/10754/344332
dc.description.abstractGlucose is the main energy substrate for the brain. There is now extensive evidence indicating that the metabolic profile of neural cells with regard to glucose utilization and glycolysis rate is not homogenous, with a marked propensity for glycolytic glucose processing in astrocytes compared to neurons. Methylglyoxal, a highly reactive dicarbonyl compound, is inevitably formed as a by-product of glycolysis. Methylglyoxal is a major cell-permeant precursor of advanced glycation end-products (AGEs), which are associated with several pathologies including diabetes, aging and neurodegenerative diseases. In normal situations, cells are protected against methylglyoxal toxicity by different mechanisms and in particular the glyoxalase system, which represents the most important pathway for the detoxification of methylglyoxal. While the neurotoxic effects of methylglyoxal and AGEs are well characterized, our understanding the glyoxalase system in the brain is more scattered. Considering the high energy requirements (i.e., glucose) of the brain, one should expect that the cerebral glyoxalase system is adequately fitted to handle methylglyoxal toxicity. This review focuses on our actual knowledge on the cellular aspects of the glyoxalase system in brain cells, in particular with regard to its activity in astrocytes and neurons. A main emerging concept is that these two neural cell types have different and energetically adapted glyoxalase defense mechanisms which may serve as protective mechanism against methylglyoxal-induced cellular damage.
dc.description.sponsorshipThis work was supported by grants from Swiss National Science Foundation (FNRS) (no. 310030B-148169/1), from the NCCR Synapsy and from the Biaggi and Panacée Foundations to Pierre J. Magistretti.
dc.language.isoen
dc.publisherFrontiers Media SA
dc.relation.urlhttp://www.frontiersin.org/Neuroenergetics%2c_Nutrition_and_Brain_Health/10.3389/fnins.2015.00023/abstract
dc.rights© 2015 Allaman, Bélanger and Magistretti. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.subjectmethylglyoxal
dc.subjectneuron
dc.subjectastrocyte
dc.subjecttriosephosphate
dc.subjectadvanced-glycation end-products (AGEs)
dc.subjectglutathione
dc.titleMethylglyoxal, the dark side of glycolysis
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentBioscience Program
dc.identifier.journalFrontiers in Neuroscience
dc.identifier.pmcidPMC4321437
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionLaboratory of Neuroenergetics and Cellular Dynamics, Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)
kaust.personMagistretti, Pierre J.
refterms.dateFOA2018-06-14T04:41:54Z


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