ReviewMetabolic brain disease2015
Does abnormal glycogen structure contribute to increased susceptibility to seizures in epilepsy?
Review in Metabolic brain disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Neuronal hyperexcitability: A key to unraveling hippocampal synaptic dysfunction in Lafora disease.Epilepsia · 2026Article
- Adeno-Associated Virus-Based Gene Therapy for Lafora Disease inInternational journal of molecular sciences · 2025Article
- Implications of aCurrent issues in molecular biology · 2024Article
- Neurovascular coupling is optimized to compensate for the increase in proton production from nonoxidative glycolysis and glycogenolysis during brain activation and maintain homeostasis of pH, pCOJournal of neurochemistry · 2024Article
- Brain energy metabolism: A roadmap for future research.Journal of neurochemistry · 2024Review
- Current state of the epilepsy drug and device pipeline.Epilepsia · 2024Review
- Exploring Astrocyte-Mediated Mechanisms in Sleep Disorders and Comorbidity.Biomedicines · 2023Review
- Role of Astrocytes in the Pathophysiology of Lafora Disease and Other Glycogen Storage Disorders.Cells · 2023Review
- Potential new roles for glycogen in epilepsy.Epilepsia · 2023Review
- Role of astrocytes in sleep deprivation: accomplices, resisters, or bystanders?Frontiers in cellular neuroscience · 2023Review
- Glial Contributions to Lafora Disease: A Systematic Review.Biomedicines · 2022Review
- Brain glycogen content is increased in the acute and interictal chronic stages of the mouse pilocarpine model of epilepsy.Epilepsia open · 2022Article
- Lack of Astrocytic Glycogen Alters Synaptic Plasticity but Not Seizure Susceptibility.Molecular neurobiology · 2020Article
- Neuromodulation of Glial Function During Neurodegeneration.Frontiers in cellular neuroscience · 2020Article
- How glycogen sustains brain function: A plausible allosteric signaling pathway mediated by glucose phosphates.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Review
- Abnormal glycogen storage in tuberous sclerosis complex caused by impairment of mTORC1-dependent and -independent signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Glycogen in Astrocytes and Neurons: Physiological and Pathological Aspects.Advances in neurobiology · 2019Review
- Review
- Astrocytic glycogen metabolism in the healthy and diseased brain.The Journal of biological chemistry · 2018Review
- Lafora disease offers a unique window into neuronal glycogen metabolism.The Journal of biological chemistry · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Epilepsy is a family of brain disorders with a largely unknown etiology and high percentage of pharmacoresistance. The clinical manifestations of epilepsy are seizures, which originate from aberrant neuronal synchronization and hyperexcitability. Reactive astrocytosis, a hallmark of the epileptic tissue, develops into loss-of-function of glutamine synthetase, impairment of glutamate-glutamine cycle and increase in extracellular and astrocytic glutamate concentration. Here, we argue that chronically elevated intracellular glutamate level in astrocytes is instrumental to alterations in the metabolism of glycogen and leads to the synthesis of polyglucosans. Unaccessibility of glycogen-degrading enzymes to these insoluble molecules compromises the glycogenolysis-dependent reuptake of extracellular K(+) by astrocytes, thereby leading to increased extracellular K(+) and associated membrane depolarization. Based on current knowledge, we propose that the deterioration in structural homogeneity of glycogen particles is relevant to disruption of brain K(+) homeostasis and increased susceptibility to seizures in epilepsy.
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What OpenQuestion holds
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.