AI Article Synopsis
- Metabolic regulation of neuronal excitability plays a key role in the development and management of seizures, suggesting that modifying energy pathways could help control epilepsy.
- The ketogenic diet, which reduces glycolysis, may provide anticonvulsant effects, particularly through the use of 2-deoxy-D-glucose (2DG), a glucose analog that inhibits glycolysis.
- Research shows that 2DG decreases seizure frequency in various models and slows the progression of kindled seizures, displaying a promising toxicity profile that could lead to new epilepsy treatments.
Article Abstract
Metabolic regulation of neuronal excitability is increasingly recognized as a factor in seizure pathogenesis and control. Inhibiting or bypassing glycolysis may be one way through which the ketogenic diet provides an anticonvulsant effect. 2-deoxy-D-glucose (2DG), a nonmetabolizable glucose analog that partially inhibits glycolysis, was tested in several acute and chronic seizure models. Acutely, 2DG decreases the frequency of high-K(+)-, bicuculline- and 4-aminopyridine-induced interictal bursts in the CA3 region of hippocampal slices; 2DG also exerts anticonvulsant effects in vivo against perforant path kindling in rats. Chronically, 2DG has novel antiepileptic effects by retarding the progression of kindled seizures. Finally, 2DG has a favorable preliminary toxicity profile. These factors support the possibility that 2DG or other modifiers of glycolysis can be used as novel treatments for epilepsy.
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| http://dx.doi.org/10.1111/j.1528-1167.2008.01848.x | DOI Listing |
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