Trial reportRedox report : communications in free radical research2011
Oxidative stress in Rett syndrome: natural history, genotype, and variants.
Trial report in Redox report : communications in free radical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed, 71 citations in OpenAlex.
- Effects of ω-3 PUFAs supplementation on myocardial function and oxidative stress markers in typical Rett syndrome.Mediators of inflammation · 2014Trial
- A randomized double blind placebo controlled clinical trial of N-Acetylcysteine added to risperidone for treating autistic disorders.BMC psychiatry · 2013Trial
- Unveiling Molecular Dynamics of MeCp2, CDKL5 and BDNF in the Hippocampus of Individuals With Intractable Mesial Temporal Lobe Epilepsy.Journal of cellular and molecular medicine · 2025Article
- Comprehensive High-Depth Proteomic Analysis of Plasma Extracellular Vesicles Containing Preparations in Rett Syndrome.Biomedicines · 2024Article
- Diet and Nutrients in Rare Neurological Disorders: Biological, Biochemical, and Pathophysiological Evidence.Nutrients · 2024Review
- Modulation of Brain Cholesterol Metabolism through CYP46A1 Overexpression for Rett Syndrome.Pharmaceutics · 2024Article
- A narrative review of the mechanisms and consequences of intermittent hypoxia and the role of advanced analytic techniques in pediatric autonomic disorders.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Association of Oxidative Stress with Neurological Disorders.Current neuropharmacology · 2022Article
- Breathing disturbances in Rett syndrome.Handbook of clinical neurology · 2022Review
- Sex disparate gut microbiome and metabolome perturbations precede disease progression in a mouse model of Rett syndrome.Communications biology · 2021Article
- How Robust is the Evidence for a Role of Oxidative Stress in Autism Spectrum Disorders and Intellectual Disabilities?Journal of autism and developmental disorders · 2021Review
- The Pathophysiology of Rett Syndrome With a Focus on Breathing Dysfunctions.Physiology (Bethesda, Md.) · 2020Review
- Treating Rett syndrome: from mouse models to human therapies.Mammalian genome : official journal of the International Mammalian Genome Society · 2019Review
- Clusterin in Alzheimer's Disease: Mechanisms, Genetics, and Lessons From Other Pathologies.Frontiers in neuroscience · 2019Review
- Mitochondrial Electron Transport Chain Complex Dysfunction in MeCP2 Knock-Down Astrocytes: Protective Effects of Quercetin Hydrate.Journal of molecular neuroscience : MN · 2019Article
- MeCP2 isoform e1 mutant mice recapitulate motor and metabolic phenotypes of Rett syndrome.Human molecular genetics · 2018Article
- Key issues in Rett syndrome: emotional, behavioural and autonomic dysregulation (EBAD) - a target for clinical trials.Orphanet journal of rare diseases · 2018Review
- Isoprostanoids in Clinical and Experimental Neurological Disease Models.Antioxidants (Basel, Switzerland) · 2018Review
- Rett syndrome: a neurological disorder with metabolic components.Open biology · 2018Review
- Oxygen exchange and energy metabolism in erythrocytes of Rett syndrome and their relationships with respiratory alterations.Molecular and cellular biochemistry · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesRett syndrome (RTT) is an X-linked autism spectrum disorder caused by mutations in the MeCP2 gene in the great majority of cases. Evidence suggests a potential role of oxidative stress (OS) in its pathogenesis. Here, we investigated the potential value of OS markers (non-protein-bound iron (NPBI) and F2-isoprostanes (F2-IsoPs)) in explaining natural history, genotype-phenotype correlation, and clinical heterogeneity of RTT, and gauging the response to omega-3 polyunsaturated fatty acids (ω-3 PUFAs).
methodsRTT patients (n=113) and healthy controls were assayed for plasma NPBI and F2-IsoPs, and intraerythrocyte NPBI. Forty-two patients with typical RTT were randomly assigned to ω-3 PUFAs supplementation for 12 months. NPBI was measured by HPLC and F2-IsoPs using a gas chromatography/negative ion chemical ionization tandem mass spectrometry (GC/NICI-MS/MS) technique.
resultsF2-IsoPs were significantly higher in the early stages as compared with the late natural progression of classic RTT. MeCP2 mutations related to more severe phenotypes exhibited higher OS marker levels than those of milder phenotypes. Higher OS markers were observed in typical RTT and early seizure variant as compared with the preserved speech and congenital variants. Significant reduction in OS markers levels and improvement of severity scores were observed after ω-3 PUFAs supplementation. DISCUSSION: OS is a key modulator of disease expression in RTT.
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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.