ArticleScience translational medicine2014
Neonatal estradiol stimulation prevents epilepsy in Arx model of X-linked infantile spasms syndrome.
Article in Science translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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Who cites it
40 citing papers in PubMed, 70 citations in OpenAlex.
- Estradiol modulates neuronal network hyperexcitability in select NDD risk genes.bioRxiv : the preprint server for biology · 2026Article
- Ketogenic diet for infantile epileptic spasms.Epilepsia open · 2025Article
- Cannabidiol attenuates epileptic phenotype and increases survival in a mouse model of developmental and epileptic encephalopathy type 1.Epilepsia · 2025Article
- Prenatal betamethasone-postnatal N-methyl-D-aspartic acid model of spasms: Update on mechanisms and treatments.Epilepsia open · 2025Article
- Article
- A comparative view of human and mouse telencephalon inhibitory neuron development.Development (Cambridge, England) · 2025Review
- Efficacy and tolerability of celastrol and edaravone in the multiple-hit rat model of infantile spasms.Epilepsy & behavior : E&B · 2025Article
- IGF2BP2-Shox2 axis regulates hippocampal-neuronal senescence to alleviate microgravity-induced recognition disturbance.iScience · 2024Article
- Genetic Advancements in Infantile Epileptic Spasms Syndrome and Opportunities for Precision Medicine.Genes · 2024Review
- Revisiting the concept of drug-resistant epilepsy: A TASK1 report of the ILAE/AES Joint Translational Task Force.Epilepsia · 2023Article
- Epileptic spasms in infancy: Transferring rat prenatal betamethasone-postnatal NMDA model to mice.Neuroscience letters · 2023Article
- Cortical Parvalbumin-Positive Interneuron Development and Function Are Altered in the APC Conditional Knockout Mouse Model of Infantile and Epileptic Spasms Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Developmental and epileptic encephalopathies: from genetic heterogeneity to phenotypic continuum.Physiological reviews · 2023Review
- Transcription factors are potential therapeutic targets in epilepsy.Journal of cellular and molecular medicine · 2022Review
- 2-deoxyglucose and β-hydroxybutyrate fail to attenuate seizures in the betamethasone-NMDA model of infantile spasms.Epilepsia open · 2022Article
- The Transcription Factor Shox2 Shapes Neuron Firing Properties and Suppresses Seizures by Regulation of Key Ion Channels in Thalamocortical Neurons.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- A team science approach to discover novel targets for infantile spasms (IS).Epilepsia open · 2021Article
- X-linked serotonin 2C receptor is associated with a non-canonical pathway for sudden unexpected death in epilepsy.Brain communications · 2021Article
- Signaling Pathways and Sex Differential Processes in Autism Spectrum Disorder.Frontiers in psychiatry · 2021Review
- Modeling epileptic spasms during infancy: Are we heading for the treatment yet?Pharmacology & therapeutics · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Infantile spasms are a catastrophic form of pediatric epilepsy with inadequate treatment. In patients, mutation of ARX, a transcription factor selectively expressed in neuronal precursors and adult inhibitory interneurons, impairs cell migration and causes a major inherited subtype of the disease X-linked infantile spasms syndrome. Using an animal model, the Arx((GCG)10+7) mouse, we determined that brief estradiol (E2) administration during early postnatal development prevented spasms in infancy and seizures in adult mutants. E2 was ineffective when delivered after puberty or 30 days after birth. Early E2 treatment altered mRNA levels of three downstream targets of Arx (Shox2, Ebf3, and Lgi1) and restored depleted interneuron populations without increasing GABAergic synaptic density. Postnatal E2 treatment may induce lasting transcriptional changes that lead to enduring disease modification and could potentially serve as a therapy for inherited interneuronopathies.
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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.