ArticleThe Journal of clinical investigation2008
Adenosine kinase is a target for the prediction and prevention of epileptogenesis in mice.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 158 papers.
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Who cites it
158 citing papers in PubMed, 252 citations in OpenAlex.
- Single-nucleus transcriptomic analysis reveals subfield-specific cell-to-cell synaptic reorganisation of the mouse hippocampus in focal temporal lobe epilepsy.Journal of translational medicine · 2026Article
- Emerging Roles of Adenosine Metabolism in Astrocytes During Brain Injury.CNS neuroscience & therapeutics · 2026Review
- Attenuated Single Neuron and Network Hyperexcitability Following MicroRNA-134 Inhibition in Mice with Drug-Resistant Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Therapeutic Potential Target of Adenosine for Epilepsy: Focusing on Its Interaction with the Molecular Epileptogenic Network.Biomolecules · 2026Review
- Calponin-3 is associated with epilepsy through the regulation of astrocyte activity.Brain pathology (Zurich, Switzerland) · 2026Article
- Anti-seizure potential of J4, an equilibrative nucleoside transporter 1 inhibitor, in a mouse model of tuberous sclerosis complex in response to pentylenetetrazol.Cell & bioscience · 2026Article
- The interplay between metabolism and neuroinflammation in epilepsy: mechanisms and therapeutic perspectives.Journal of neuroinflammation · 2025Review
- Article
- Astrocyte-Neuron Metabolic Synergies in Neurological Homeostasis and Disease.Neurochemical research · 2025Review
- Hyperibone J exerts antidepressant effects by targeting ADK to inhibit microglial P2X7R/TLR4-mediated neuroinflammation.Journal of advanced research · 2025Article
- Adenosine Kinase: An Epigenetic Modulator and Drug Target.Journal of inherited metabolic disease · 2025Review
- Deep Brain Stimulation Inhibits Epileptic Seizures via Increase of Adenosine Release and Inhibition of ENT1, CD39, and CD73 Expression.Molecular neurobiology · 2025Article
- Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025Review
- Article
- Neuroregeneration Improved by Sodium-D,L-Beta-Hydroxybutyrate in Primary Neuronal Cultures.Pharmaceuticals (Basel, Switzerland) · 2024Article
- The immune system and metabolic products in epilepsy and glioma-associated epilepsy: emerging therapeutic directions.JCI insight · 2024Review
- Deep brain stimulation suppresses epileptic seizures in rats via inhibition of adenosine kinase and activation of adenosine A1 receptors.CNS neuroscience & therapeutics · 2023Article
- Ectopic expression of neuronal adenosine kinase, a biomarker in mesial temporal lobe epilepsy without hippocampal sclerosis.Neuropathology and applied neurobiology · 2023Article
- Aberrant adenosine signaling in patients with focal cortical dysplasia.Molecular neurobiology · 2023Article
- Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023Review
98 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Astrogliosis is a pathological hallmark of the epileptic brain. The identification of mechanisms that link astrogliosis to neuronal dysfunction in epilepsy may provide new avenues for therapeutic intervention. Here we show that astrocyte-expressed adenosine kinase (ADK), a key negative regulator of the brain inhibitory molecule adenosine, is a potential predictor and modulator of epileptogenesis. In a mouse model of focal epileptogenesis, in which astrogliosis is restricted to the CA3 region of the hippocampus, we demonstrate that upregulation of ADK and spontaneous focal electroencephalographic seizures were both restricted to the affected CA3. Furthermore, spontaneous seizures in CA3 were mimicked in transgenic mice by overexpression of ADK in this brain region, implying that overexpression of ADK without astrogliosis is sufficient to cause seizures. Conversely, after pharmacological induction of an otherwise epileptogenesis-precipitating acute brain injury, transgenic mice with reduced forebrain ADK were resistant to subsequent epileptogenesis. Likewise, ADK-deficient ES cell-derived brain implants suppressed astrogliosis, upregulation of ADK, and spontaneous seizures in WT mice when implanted after the epileptogenesis-precipitating brain injury. Our findings suggest that astrocyte-based ADK provides a critical link between astrogliosis and neuronal dysfunction in 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.