Comparison of HMGB1, RAGE, TLR4, and NF-κB levels in children and adolescents diagnosed with autism spectrum disorder with healthy controls.

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...

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Bibliographic Details
Published in:International Journal of Developmental Disabilities Vol. 71; no. 7; pp. 1073 - 1081
Main Authors: Kıyat, Esra, Aktepe, Evrim, Kumbul Doğuç, Duygu, Bedir, Mehmet, Ertürk, Emre, Işık, Ümit
Format: research tables/charts Journal Article
Published: Taylor & Francis Ltd Nov2025
Online Access:View this record in EBSCOhost
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Summary: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 (p < 0.001), other parameters examined did not show significant differences between groups. Furthermore, soluble TLR4 serum level was positively correlated with Problem Behavior Checklist hyperactivity subscale scores (p = 0.031), and RAGE serum level was negatively correlated with ABC Stereotype score (p = 0.001). 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.