ArticleMediators of inflammation2014
Subclinical inflammatory status in Rett syndrome.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 67 citations in OpenAlex.
- Leptin antagonism improves Rett syndrome phenotype in symptomatic Mecp2-deficient mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
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- The methyl-CpG-binding protein 2 inhibits cGAS-associated signaling.Nature communications · 2025Article
- Epigenetic Mechanisms in Fabry Disease: A Thematic Analysis Linking Differential Methylation Profiles and Genetic Modifiers to Disease Phenotype.Current issues in molecular biology · 2025Review
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- Comprehensive High-Depth Proteomic Analysis of Plasma Extracellular Vesicles Containing Preparations in Rett Syndrome.Biomedicines · 2024Article
- Mitochondrial modulation with leriglitazone as a potential treatment for Rett syndrome.Journal of translational medicine · 2023Article
- Advances in the pathogenesis of Rett syndrome using cell models.Animal models and experimental medicine · 2022Review
- Proteomic and transcriptional changes associated with MeCP2 dysfunction reveal nodes for therapeutic intervention in Rett syndrome.Neurochemistry international · 2021Review
- MeCP2 deficiency exacerbates the neuroinflammatory setting and autoreactive response during an autoimmune challenge.Scientific reports · 2021Article
- Unraveling Molecular Pathways Altered in MeCP2-Related Syndromes, in the Search for New Potential Avenues for Therapy.Biomedicines · 2021Article
- Patient-derived iPSC modeling of rare neurodevelopmental disorders: Molecular pathophysiology and prospective therapies.Neuroscience and biobehavioral reviews · 2021Review
- Rett syndrome: think outside the (skull) box.Faculty reviews · 2021Review
- Comprehensive Analysis of GABAInternational journal of molecular sciences · 2020Article
- Evidence of altered salivary cytokine concentrations in Rett syndrome and associations with clinical severity.Brain, behavior, & immunity - health · 2020Article
- Complement System in Brain Architecture and Neurodevelopmental Disorders.Frontiers in neuroscience · 2020Review
- Altered trajectories of neurodevelopment and behavior in mouse models of Rett syndrome.Neurobiology of learning and memory · 2019Review
- Article
- Transposable Elements, Inflammation, and Neurological Disease.Frontiers in neurology · 2019Review
- Transcriptomic Analysis ofFrontiers in psychiatry · 2019Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation has been advocated as a possible common central mechanism for developmental cognitive impairment. Rett syndrome (RTT) is a devastating neurodevelopmental disorder, mainly caused by de novo loss-of-function mutations in the gene encoding MeCP2. Here, we investigated plasma acute phase response (APR) in stage II (i.e., "pseudo-autistic") RTT patients by routine haematology/clinical chemistry and proteomic 2-DE/MALDI-TOF analyses as a function of four major MECP2 gene mutation types (R306C, T158M, R168X, and large deletions). Elevated erythrocyte sedimentation rate values (median 33.0 mm/h versus 8.0 mm/h, P < 0.0001) were detectable in RTT, whereas C-reactive protein levels were unchanged (P = 0.63). The 2-DE analysis identified significant changes for a total of 17 proteins, the majority of which were categorized as APR proteins, either positive (n = 6 spots) or negative (n = 9 spots), and to a lesser extent as proteins involved in the immune system (n = 2 spots), with some proteins having overlapping functions on metabolism (n = 7 spots). The number of protein changes was proportional to the severity of the mutation. Our findings reveal for the first time the presence of a subclinical chronic inflammatory status related to the "pseudo-autistic" phase of RTT, which is related to the severity carried by the MECP2 gene mutation.
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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.