ReviewNature neuroscience2016
Glia as drivers of abnormal neuronal activity.
Review in Nature neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
118 citing papers in PubMed, 1 synthesis or guideline pooled it, 194 citations in OpenAlex.
- Pooled it
- Clinical application of artificial intelligence technology in epilepsy.Acta epileptologica · 2026Review
- The role of Annexin A2 in Alzheimer's disease: From cellular functions to therapeutic potential.The FEBS journal · 2026Review
- Light- and temperature-sensitive seizures are regulated by spatially distinct cortex glial populations in the central nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Apoptosis and Glial Marker Profiles in Hippocampus and Amygdala of Medically Intractable Temporal Lobe Epilepsy.Journal of cellular and molecular medicine · 2026Article
- PARP1-TRPM2-PKC cascade distinctly regulates reactive astrogliosis and clasmatodendrosis through NF-κB and AKT pathways in the hippocampus of chronic epilepsy rats.Scientific reports · 2025Article
- Astrocyte Interactions With TiAdvanced materials interfaces · 2025Article
- Fenofibrate as a PPARα Agonist Modulates Neuroinflammation and Glutamate Receptors in a Rat Model of Temporal Lobe Epilepsy: Region-Specific Effects and Behavioral Outcomes.International journal of molecular sciences · 2025Article
- Tcf4 Deficiency causes recurrent seizures in mice.Progress in neurobiology · 2025Article
- Potassium homeostasis during disease progression of Alzheimer's disease.The Journal of physiology · 2025Article
- Article
- Investigating the Pathology-Related Astroglial Plasticity in the Human Cerebral Cortex.Methods in molecular biology (Clifton, N.J.) · 2025Article
- The top 100 most cited publications on astrocytes in Alzheimer's disease from 2000 to 2025: a bibliometric analysis.Frontiers in neuroscience · 2025Article
- Neuroglia and brain energy metabolism.Handbook of clinical neurology · 2025Review
- Dorsoventral photobiomodulation therapy safely reduces inflammation and sensorimotor deficits in a mouse model of multiple sclerosis.Journal of neuroinflammation · 2024Article
- Shifts in the spatiotemporal profile of inflammatory phenotypes of innate immune cells in the rat brain following acute intoxication with the organophosphate diisopropylfluorophosphate.Journal of neuroinflammation · 2024Article
- Integrative Human Genetic and Cellular Analysis of the Pathophysiological Roles of AnxA2 in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2024Article
- PPARβ/δ Agonist GW0742 Modulates Microglial and Astroglial Gene Expression in a Rat Model of Temporal Lobe Epilepsy.International journal of molecular sciences · 2024Article
- Schwann cell-secreted PGECell · 2024Article
- Disease-relevant upregulation of P2YNature communications · 2024Article
58 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Reactive astrocytes have been proposed to become incompetent bystanders in epilepsy as a result of cellular changes rendering them unable to perform important housekeeping functions. Indeed, successful surgical treatment of mesiotemporal lobe epilepsy hinges on the removal of the glial scar. New research now extends the role of astrocytes, suggesting that they may drive the disease process by impairing the inhibitory action of neuronal GABA receptors. Here we discuss studies that include hyperexcitability resulting from impaired supply of astrocytic glutamine for neuronal GABA synthesis, and epilepsy resulting from genetically induced astrogliosis or malignant transformation, both of which render the inhibitory neurotransmitter GABA excitatory. In these examples, glial cells alter the expression or function of neuronal proteins involved in excitability. Although epilepsy has traditionally been thought of as a disease caused by changes in neuronal properties exclusively, these new findings challenge us to consider the contribution of glial cells as drivers of epileptogenesis in acquired epilepsies.
Indexed as
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.