ReviewTrends in pharmacological sciences2022
Unifying mechanism behind the onset of acquired epilepsy.
Review in Trends in pharmacological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Metabolic and redox modulation by 2-deoxy-D-glucose and sodium selenite protects against pentylenetetrazole-kindled seizures, neuroinflammation and cognitive dysfunction.Metabolic brain disease · 2026Article
- Continuous Pyruvate Supplementation Enhances Neuroprotective Resilience Against Kainate-Induced Status Epilepticus Through Metabolic Preconditioning.Biomolecules · 2026Article
- The interplay between metabolism and neuroinflammation in epilepsy: mechanisms and therapeutic perspectives.Journal of neuroinflammation · 2025Review
- Beyond Impaired GABAergic Signaling: Inflammation and Metabolic Dysfunction in Genetic Epilepsy Induced by GABRG2 Mutation.Molecular neurobiology · 2025Article
- Effects of tDCS on glutamatergic pathways in epilepsy: neuroprotective and therapeutic potential.Pflugers Archiv : European journal of physiology · 2025Article
- Astroglia's role in synchronized spontaneous neuronal activity: from physiology to pathology.Frontiers in cellular neuroscience · 2025Review
- Metabolic aspects of genetic ion channel epilepsies.Journal of neurochemistry · 2024Review
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
- The NADPH Oxidase Inhibitor, Mitoapocynin, Mitigates DFP-Induced Reactive Astrogliosis in a Rat Model of Organophosphate Neurotoxicity.Antioxidants (Basel, Switzerland) · 2023Article
- Further advances in epilepsy.Journal of neurology · 2023Review
- A narrative review of the mechanisms and consequences of intermittent hypoxia and the role of advanced analytic techniques in pediatric autonomic disorders.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Degeneracy in epilepsy: multiple routes to hyperexcitable brain circuits and their repair.Communications biology · 2023Review
- Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Potential new roles for glycogen in epilepsy.Epilepsia · 2023Review
- TRPC channels as emerging targets for seizure disorders.Trends in pharmacological sciences · 2022Review
- Metabonomic analysis of cerebrospinal fluid in epilepsy.Annals of translational medicine · 2022Article
- Crosstalk between neuroinflammation and oxidative stress in epilepsy.Frontiers in cell and developmental biology · 2022Review
- Significance of Brain Glucose Hypometabolism, Altered Insulin Signal Transduction, and Insulin Resistance in Several Neurological Diseases.Frontiers in endocrinology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
Abstract
Acquired epilepsy (AE) can result from a number of brain insults and neurological diseases with wide etiological diversity sharing one common outcome of brain epileptiform activity. This implies that despite their disparity, all these initiating pathologies affect the same fundamental brain functions underlying network excitability. Identifying such mechanisms and their availability as therapeutic targets would help develop an effective strategy for epileptogenesis prevention. In this opinion article, we propose that the vicious cycle of NADPH oxidase (NOX)-mediated oxidative stress and glucose hypometabolism is the underlying cause of AE, as available data reveal a critical role for both pathologies in epileptogenesis and the process of seizure initiation. Altogether, here we present a novel view on the mechanisms behind the onset of AE and identify therapeutic targets for potential clinical applications.
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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.