ArticleBiological psychiatry2016
Chronic Administration of the N-Methyl-D-Aspartate Receptor Antagonist Ketamine Improves Rett Syndrome Phenotype.
Article in Biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05321160 (Comparison of Esketamine Versus Sevoflurane Add to Dexmedetomidine-based Sedation for Minor Ophthalmology Procedure in Children), which is not on this map. Cited by 53 papers, 2 of them syntheses that pooled it.
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.
Comparison of Esketamine Versus Sevoflurane Add to Dexmedetomidine-based Sedation for Minor Ophthalmology Procedure in Children: A Randomized Controlled Trial.
Who cites it
53 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Efficacy and safety of esketamine in patients undergoing painless gastrointestinal endoscopy: a systematic review and meta-analysis of randomized controlled trials.Frontiers in medicine · 2025Pooled it
- Efficacy and safety of esketamine for sedation among patients undergoing gastrointestinal endoscopy: a systematic review and meta-analysis.BMC anesthesiology · 2023Pooled it
- A randomized, placebo-controlled, cross-over trial of ketamine in Rett syndrome.Journal of neurodevelopmental disorders · 2025Trial
- Median effective dose (EDBMC anesthesiology · 2023Trial
- Visual Recovery Reflects Cortical MeCP2 Sensitivity in Rett Syndrome.Annals of clinical and translational neurology · 2026Article
- MECP2 Dysfunction in Rett Syndrome: Molecular Mechanisms, Multisystem Pathology, and Emerging Therapeutic Strategies.International journal of molecular sciences · 2025Review
- MeCP2 prevents against sustained ketamine-induced synaptic depression at inhibitory synapses.iScience · 2025Article
- Potentiation of group III metabotropic glutamate receptors positively affects neurophysiological features in a mouse model of Rett syndrome.The Journal of pharmacology and experimental therapeutics · 2025Article
- Effect of esketamine on the ECiScience · 2025Article
- Intravenous esketamine in pediatric Rett syndrome: An open-label, early phase 1 pilot study.Molecular therapy. Methods & clinical development · 2025Article
- Article
- Targeting Sigma Receptors for the Treatment of Neurodegenerative and Neurodevelopmental Disorders.CNS drugs · 2023Review
- Cell-specific vulnerability to metabolic failure: the crucial role of parvalbumin expressing neurons in creatine transporter deficiency.Acta neuropathologica communications · 2023Article
- Zelquistinel Is an Orally Bioavailable Novel NMDA Receptor Allosteric Modulator That Exhibits Rapid and Sustained Antidepressant-Like Effects.The international journal of neuropsychopharmacology · 2022Article
- Selective Xi reactivation and alternative methods to restore MECP2 function in Rett syndrome.Trends in genetics : TIG · 2022Review
- Clinical and Preclinical Evidence for MNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Rett Syndrome andNeuropsychiatric disease and treatment · 2022Review
- Excitation and Inhibition Imbalance in Rett Syndrome.Frontiers in neuroscience · 2022Review
- Reviewing Evidence for the Relationship of EEG Abnormalities and RTT Phenotype Paralleled by Insights from Animal Studies.International journal of molecular sciences · 2021Review
- The enhancement of activity rescues the establishment of Mecp2 null neuronal phenotypes.EMBO molecular medicine · 2021Article
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7 authors.
Funding
Abstract
backgroundRett syndrome (RTT) is a neurological disorder caused by mutation of the X-linked MECP2 gene, which results in the progressive disruption of excitatory and inhibitory neuronal circuits. To date, there is no effective treatment available for the disorder. Studies conducted in RTT patients and murine models have shown altered expression of N-methyl-D-aspartate receptors (NMDARs). Genetic deletion of the NMDAR subunit, GluN2A, in mice lacking Mecp2 is sufficient to prevent RTT phenotypes, including regression of vision.
methodsWe performed a systematic, randomized preclinical trial of chronic administration of low-dose (8 mg/kg, intraperitoneal) ketamine, an NMDAR antagonist, starting either early in development or at the onset of RTT phenotype in Mecp2-null mice.
resultsDaily exposure to ketamine ameliorated RTT symptoms and extended the life span of treated Mecp2-null mice without adverse side effects. Furthermore, significant improvement was observed in cortical processing and connectivity, which were fully restored to a wild-type level, particularly when treatment was started at the onset of regression.
conclusionsOur findings provide strong evidence that targeting NMDA receptors can be a safe and effective treatment for RTT.
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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.