ReviewFrontiers in cellular neuroscience2018
Dysregulated Glucose Metabolism as a Therapeutic Target to Reduce Post-traumatic Epilepsy.
Review in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Review
- mtDNA leakage promotes neuron-glia crosstalk to induce epilepsy by cGAS-STING-driven neuroinflammation and serine metabolic reprogramming.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Disrupted Vitamin D Signaling and Metabolism in Neurodevelopmental and Neurodegenerative Disorders.ASN neuro · 2026Review
- Functional characterization of a human epilepsy-associated gene network reveals metabolic regulation as a critical factor underlying seizure susceptibilities.Disease models & mechanisms · 2026Article
- The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.Neuroscience bulletin · 2025Review
- Brain Glucose Hypometabolism and Brain Iron Accumulation as Therapeutic Targets for Alzheimer's Disease and Other CNS Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Alterations in topology, cost, and dynamics of gamma-band EEG functional networks in a preclinical model of traumatic brain injury.Network neuroscience (Cambridge, Mass.) · 2025Article
- Development of a novel glucose-dendrimer based therapeutic targeting hyperexcitable neurons in neurological disorders.Bioengineering & translational medicine · 2024Article
- Tracing the path of disruption:CNS neuroscience & therapeutics · 2024Review
- Early hippocampal high-amplitude rhythmic spikes predict post-traumatic epilepsy in mice.Frontiers in neuroscience · 2024Article
- Broadband-NIRS System Identifies Epileptic Focus in a Child with Focal Cortical Dysplasia-A Case Study.Metabolites · 2022Article
- Novel Approaches to Prevent Epileptogenesis After Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Review
- Article
- In Vivo Imaging of Neuroinflammatory Targets in Treatment-Resistant Epilepsy.Current neurology and neuroscience reports · 2020Review
- Glycolytic inhibitor 2-deoxyglucose prevents cortical hyperexcitability after traumatic brain injury.JCI insight · 2019Article
- Epilepsy Benchmarks Area II: Prevent Epilepsy and Its Progression.Epilepsy currentsArticle
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Traumatic brain injury (TBI) is a significant cause of disability worldwide and can lead to post-traumatic epilepsy. Multiple molecular, cellular, and network pathologies occur following injury which may contribute to epileptogenesis. Efforts to identify mechanisms of disease progression and biomarkers which predict clinical outcomes have focused heavily on metabolic changes. Advances in imaging approaches, combined with well-established biochemical methodologies, have revealed a complex landscape of metabolic changes that occur acutely after TBI and then evolve in the days to weeks after. Based on this rich clinical and preclinical data, combined with the success of metabolic therapies like the ketogenic diet in treating epilepsy, interest has grown in determining whether manipulating metabolic activity following TBI may have therapeutic value to prevent post-traumatic epileptogenesis. Here, we focus on changes in glucose utilization and glycolytic activity in the brain following TBI and during seizures. We review relevant literature and outline potential paths forward to utilize glycolytic inhibitors as a disease-modifying therapy for post-traumatic epilepsy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.