ArticleNature neuroscience2024
Targeting pathological cells with senolytic drugs reduces seizures in neurodevelopmental mTOR-related epilepsy.
Article in Nature neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02890641 (Genetic and Electrophysiologic Study in Focal Drug-resistant Epilepsies), which is not on this map. Cited by 30 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.
Genetic and Electrophysiologic Study in Focal Drug-resistant Epilepsies
Who cites it
30 citing papers in PubMed.
- The role of senescence in kidney ageing, injury and fibrosis.Nature reviews. Nephrology · 2026Review
- Mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE): genetics, mechanisms and precision therapy.Acta neuropathologica · 2026Review
- Research progress of traditional Chinese medicine interventions for aging-related nervous system diseases.Biogerontology · 2026Review
- Targeted senotherapy improves electrographic and behavioral outcomes in a mouse model of temporal lobe epilepsy.Epilepsia · 2026Article
- Targeted interneuron ablation in an mTORopathy model: Testing a two-hit mechanism of epileptogenesis.Progress in neurobiology · 2026Article
- Neuroinflammation in Epilepsy: Biochemical and Molecular Mechanisms and Implications for Natural Product-Driven Drug Discovery.International journal of molecular sciences · 2026Review
- Senescent Cell Clearance Ameliorates Temporal Lobe Epilepsy and Associated Spatial Memory Deficits in Mice.Annals of neurology · 2026Article
- Quercetin as a multifaceted neuroprotective agent against cerebral ischaemia-reperfusion injury: mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Gastrodin alleviates neuronal damage in epileptic cell models by targeting P2RY12 to inhibit microglial hyperactivation.PloS one · 2026Article
- The senescent niche hypothesis: microglial dysfunction and replacement strategies in drug-resistant epilepsy.Frontiers in immunology · 2026Review
- Dasatinib and Quercetin Alleviate Retinal Ganglion Cell Dendritic Shrinkage and Promote Axonal Regeneration in Mice with Optic Nerve Injury.International journal of molecular sciences · 2025Article
- Seizure occurrence in FCD type II is predicted by lesion position and linked to cytoarchitectural alterations.Acta neuropathologica communications · 2025Article
- Ablation of dysmorphic neurons is a safe and effective treatment for focal cortical dysplasia II.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Epilepsy and autophagy modulators: a therapeutic split.Autophagy · 2025Review
- Cortical Dysplasia Beyond mTOR: Cellular Senescence Takes a Toll.Neuroscience bulletin · 2025Article
- Single-cell genotyping and transcriptomic profiling of mosaic focal cortical dysplasia.Nature neuroscience · 2025Article
- Neuronal autophagy controls excitability via ryanodine receptor-mediated regulation of calcium-activated potassium channel function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transcriptomic and morphologic vascular aberrations underlying FCDIIb etiology.Nature communications · 2025Article
- Targeting senescent hepatocytes for treatment of metabolic dysfunction-associated steatotic liver disease and multi-organ dysfunction.Nature communications · 2025Article
- Disease modification upon 2 weeks of tofacitinib treatment in a mouse model of chronic epilepsy.Science translational medicine · 2025Article
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16 authors.
Funding
Abstract
Cortical malformations such as focal cortical dysplasia type II (FCDII) are associated with pediatric drug-resistant epilepsy that necessitates neurosurgery. FCDII results from somatic mosaicism due to post-zygotic mutations in genes of the PI3K-AKT-mTOR pathway, which produce a subset of dysmorphic cells clustered within healthy brain tissue. Here we show a correlation between epileptiform activity in acute cortical slices obtained from human surgical FCDII brain tissues and the density of dysmorphic neurons. We uncovered multiple signatures of cellular senescence in these pathological cells, including p53/p16 expression, SASP expression and senescence-associated β-galactosidase activity. We also show that administration of senolytic drugs (dasatinib/quercetin) decreases the load of senescent cells and reduces seizure frequency in an Mtor
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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.