ArticleNeuron2012
BAD-dependent regulation of fuel metabolism and K(ATP) channel activity confers resistance to epileptic seizures.
Article in Neuron, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.
- The Efficacy of Ketogenic Therapies in the Clinical Management of People with Neurodegenerative Disease: A Systematic Review.Advances in nutrition (Bethesda, Md.) · 2021Pooled it
- Review
- Passive neuromodulation: an energy-driven mechanism for closed-loop suppression of epileptic seizures.bioRxiv : the preprint server for biology · 2026Article
- Article
- Mitochondrial membrane junction-mediated ATP channeling drives activity-dependent glucose metabolism.bioRxiv : the preprint server for biology · 2025Article
- Providing alternative fuel for the brain in anorexia nervosa: a review of the literature on ketones and their effects on metabolism and the brain.Translational psychiatry · 2025Review
- Impact of the Ketogenic Diet on Neurological Diseases: A Review.Life (Basel, Switzerland) · 2025Review
- Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025Review
- Neuronal activity-driven O-GlcNAcylation promotes mitochondrial plasticity.Developmental cell · 2024Article
- Novel loss-of-function variants expand ABCC9-related intellectual disability and myopathy syndrome.Brain : a journal of neurology · 2024Article
- Ketogenic Diet in the Treatment of Epilepsy.Nutrients · 2024Review
- Low glycemic index diet restrains epileptogenesis in a gender-specific fashion.Cellular and molecular life sciences : CMLS · 2023Article
- Reinventing the Penumbra - the Emerging Clockwork of a Multi-modal Mechanistic Paradigm.Translational stroke research · 2023Review
- The Influence of Ketogenic Diet on Gut Microbiota: Potential Benefits, Risks and Indications.Nutrients · 2023Review
- Regulatory Basis of Adipokines Leptin and Adiponectin in Epilepsy: from Signaling Pathways to Glucose Metabolism.Neurochemical research · 2023Review
- Involvement of a BH3-only apoptosis sensitizer gene Blm-s in hippocampus-mediated mood control.Translational psychiatry · 2022Article
- AMPK-mediated potentiation of GABAergic signalling drives hypoglycaemia-provoked spike-wave seizures.Brain : a journal of neurology · 2022Article
- The metabolic basis of epilepsy.Nature reviews. Neurology · 2022Review
- Paradoxical neuronal hyperexcitability in a mouse model of mitochondrial pyruvate import deficiency.eLife · 2022Article
- Insights into the Cellular Interactions and Molecular Mechanisms of Ketogenic Diet for Comprehensive Management of Epilepsy.Current neuropharmacology · 2022Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Neuronal excitation can be substantially modulated by alterations in metabolism, as evident from the anticonvulsant effect of diets that reduce glucose utilization and promote ketone body metabolism. We provide genetic evidence that BAD, a protein with dual functions in apoptosis and glucose metabolism, imparts reciprocal effects on metabolism of glucose and ketone bodies in brain cells. These effects involve phosphoregulation of BAD and are independent of its apoptotic function. BAD modifications that reduce glucose metabolism produce a marked increase in the activity of metabolically sensitive K(ATP) channels in neurons, as well as resistance to behavioral and electrographic seizures in vivo. Seizure resistance is reversed by genetic ablation of the K(ATP) channel, implicating the BAD-K(ATP) axis in metabolic control of neuronal excitation and seizure responses.
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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.