ArticleThe open neuroscience journal2010
Adenosine dysfunction and adenosine kinase in epileptogenesis.
Article in The open neuroscience journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- Research progress in glioma-related epilepsy (Review).Biomedical reports · 2025Article
- Neurocognitive and neurobiological effects of low dose organophosphate exposure.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- The molecular landscape of glioblastoma-associated epilepsy.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Article
- Clinico-genetic Analysis of Adenosine Signaling Pathway in Drug-Resistant Epilepsy.Annals of Indian Academy of Neurology · 2025Article
- Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a knock in mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2024Article
- Modulation of Microglial Function by ATP-Gated P2X7 Receptors: Studies in Rat, Mice and Human.Cells · 2024Review
- Inborn Errors of Purine Salvage and Catabolism.Metabolites · 2023Review
- Astrocyte-neuron circuits in epilepsy.Neurobiology of disease · 2023Review
- A novel deep learning model for glioma epilepsy associated with the identification of human cytomegalovirus infection injuries based on head MR.Frontiers in microbiology · 2023Article
- Panx1 channels promote both anti- and pro-seizure-like activities in the zebrafish via p2rx7 receptors and ATP signaling.Communications biology · 2022Article
- Computational exploration of vicine - an alkaloid glycoside mediated pathological hallmark of adenosine kinase to promote neurological disorder.Metabolic brain disease · 2021Article
- Research progress on adenosine in central nervous system diseases.CNS neuroscience & therapeutics · 2019Review
- Understanding the Role of Adenosine A2AR Heteroreceptor Complexes in Neurodegeneration and Neuroinflammation.Frontiers in neuroscience · 2018Article
- Brain Tumor-Related Epilepsy: a Current Review of the Etiologic Basis and Diagnostic and Treatment Approaches.Current neurology and neuroscience reports · 2017Review
- The chemokine CXCL16 modulates neurotransmitter release in hippocampal CA1 area.Scientific reports · 2016Article
- Seizures and brain regulatory systems: consciousness, sleep, and autonomic systems.Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society · 2015Review
- Article
- Time to focus on brain tumor-related epilepsy trials.Neuro-oncology practice · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Traditionally, epilepsy has been considered to be a disorder of neuronal dysfunction. Based on this dogma, drug development efforts have largely focused on neurocentric model systems to screen for compounds that affect the function of neurons. Unfortunately, about 30% of all patients with epilepsy - or more than 20 million worldwide - are refractory to classical neurocentric pharmacotherapy. The failure of neurocentric pharmacotherapy in epilepsy requires radical rethinking and the search for novel therapeutic targets. Research from recent years suggests that epilepsy is a disorder of astrocyte dysfunction. Astrocytes are key regulators of the brain's own anticonvulsant adenosine. Thus, any dysfunction in astrocyte metabolism will drastically affect the brain's ability to control excitability via adenosinergic neuromodulation. This review will focus on the astrocyte-based enzyme adenosine kinase (ADK) as the key regulator of synaptic adenosine. Astrogliosis - a pathological hallmark of the epileptic brain - leads to overexpression of the adenosine-removing enzyme ADK and therefore to adenosine deficiency. Evidence from transgenic animals demonstrates that overexpression of ADK per se is sufficient to trigger seizures. Consequently, pharmacological inhibition of ADK is very effective in suppressing seizures that are refractory to classical antiepileptic drugs. The recent definition of ADK as rational target to predict and to prevent seizures in epilepsy has prompted the development of focal adenosine augmentation therapies (AATs) that have been designed to selectively reconstitute adenosinergic signalling within an area of astrogliosis-based adenosine-dysfunction. This therapeutic challenge has experimentally been met with polymeric or stem cell based brain implants to afford the focal delivery of adenosine.
Identifiers
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.