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. 2020 Dec 8;11:592514. doi: 10.3389/fneur.2020.592514

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Copyright © 2020 Fei, Shi, Song and Wu.

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) and the copyright owner(s) 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.

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Antiepileptic mechanism of glycolysis inhibitor 2-deoxyglucose. As a classical glycolysis inhibitor, 2-deoxyglucose (2-DG) would inhibit the energetics of glucose and decrease the ATP. Glycolysis reduction will enhance the pentose phosphate pathway (PPP) metabolism and resulting in GABAergic strength (91). On the other hand, 2-DG reduces epilepsy progression by NRSF–dependent metabolic regulation of BDNF and TrkB (11). Glc, glucose; G-6-P, glucose-6-phosphate; 2-DG-6-P, 2-deoxyglucose-6-phosphate; NRSF, neural restrictive silencing factor; BDNF, brain-derived neurotrophic factor; TrkB, tyrosine kinase receptor B; 5α-R, 5α-reductase.