Fractalkine and Neuroinflammation in Autism Spectrum Disorder: A Novel Perspective
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Objective: To investigate the role of neuroinflammation in the etiopathogenesis of autism spectrum disorder (ASD), we investigated the role of fractalkine and tumour necrosis factor alpha (TNF-), which may be potential biomarkers for ASD. This study aimed to evaluate the serum levels of interleukin-1beta (IL-1), interleukin-6 (IL-6), and high-sensitivity CRP (hs-CRP) and to investigate the relationship between fractalkine, TNF-, IL-1, IL-6, and hs-CRP and the severity of symptoms in ASD. Methods: In this cross-sectional study, 44 children between the ages of 24−72 months diagnosed with ASD constituted the research group, and 44 healthy children of similar age and sex constituted the control group. Detailed mental status examinations were performed in both groups. Symptom severity of children diagnosed with ASD was evaluated using the Childhood Autism Rating Scale, Autism Behaviour Checklist and Repetitive Behaviours Scale-Revised Turkish Version. Peripheral venous blood samples were obtained from children in both groups and serum fractalkine, TNF-, IL-1, IL-6 and hs-CRP levels were measured by ELISA method. Results: Serum fractalkine and IL-1 levels of children in the ASD group were significantly lower than those in the control group. No significant difference was found between the groups in serum TNF-, IL-6 and hs-CRP levels. There was no correlation between ASD severity and fractalkine, TNF-, IL-1, and IL-6 levels. Conclusion: Our study is the first to evaluate serum fractalkine levels in ASD in early childhood. Our findings suggest that fractalkine may play a role in the etiopathogenesis of ASD in early life and may be a potential biomarker for ASD.
Abstract
Objective: To investigate the role of neuroinflammation in the etiopathogenesis of autism spectrum disorder (ASD), we investigated the role of fractalkine and tumour necrosis factor alpha (TNF-), which may be potential biomarkers for ASD. This study aimed to evaluate the serum levels of interleukin-1beta (IL-1), interleukin-6 (IL-6), and high-sensitivity CRP (hs-CRP) and to investigate the relationship between fractalkine, TNF-, IL-1, IL-6, and hs-CRP and the severity of symptoms in ASD. Methods: In this cross-sectional study, 44 children between the ages of 24−72 months diagnosed with ASD constituted the research group, and 44 healthy children of similar age and sex constituted the control group. Detailed mental status examinations were performed in both groups. Symptom severity of children diagnosed with ASD was evaluated using the Childhood Autism Rating Scale, Autism Behaviour Checklist and Repetitive Behaviours Scale-Revised Turkish Version. Peripheral venous blood samples were obtained from children in both groups and serum fractalkine, TNF-, IL-1, IL-6 and hs-CRP levels were measured by ELISA method. Results: Serum fractalkine and IL-1 levels of children in the ASD group were significantly lower than those in the control group. No significant difference was found between the groups in serum TNF-, IL-6 and hs-CRP levels. There was no correlation between ASD severity and fractalkine, TNF-, IL-1, and IL-6 levels. Conclusion: Our study is the first to evaluate serum fractalkine levels in ASD in early childhood. Our findings suggest that fractalkine may play a role in the etiopathogenesis of ASD in early life and may be a potential biomarker for ASD.