ArticleInternational journal of developmental disabilities2025
Comparison of HMGB1, RAGE, TLR4, and NF-κB levels in children and adolescents diagnosed with autism spectrum disorder with healthy controls.
Article in International journal of developmental disabilities, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed.
- Serum TLR4, NF-κB, and NLRP3 Levels in Children with Attention-Deficit/Hyperactivity Disorder: A Case-Control Study.Children (Basel, Switzerland) · 2026Article
- Gut Microbiota and Autism Spectrum Disorder: A Neuroinflammatory Mediated Mechanism of Pathogenesis?Inflammation · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The objective of our study is to clarify the involvement of the HMGB1/RAGE/TLR4/NF-kB axis, a crucial component in inflammation, in the etiopathogenesis of autism spectrum disorder (ASD). Method: We analyzed the levels of HMGB1, RAGE, TLR4, and NF-kB in serum from 80 children (40 with ASD and 40 controls). All participants' sociodemographic characteristics were recorded. In order to determine the severity of the disorder, the Aberrant Behavior Checklist, Childhood Autism Rating Scale, and Autism Behavior Checklist were administered to the ASD group. Result: While the soluble TLR4 level was significantly higher in the ASD group ( Discussion: It was thought that serum TLR4 levels may be important in the etiology of ASD. TLR4 levels are linked to symptoms like hyperactivity in autism, which suggests that this parameter could be used as a clinical guide. Further research is required to substantiate our discoveries and to clarify the involvement of HMGB1, RAGE, TLR4, and NF-kB in the etiopathogenesis of ASD.
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Registered trials
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