Publication date: May 22, 2025

Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by impairments in social communication, repetitive behaviors, and restricted interests. Emerging evidence suggests that immune system dysregulation, particularly alterations in the complement system, may contribute to ASD pathophysiology. This study aimed to compare the serum levels of complement proteins (C1q, C2, C3, C4, MBL, L-Ficolin and hsCRP) between children with ASD and non-ASD controls. A total of 88 children (44 with ASD and 44 age- and sex-matched healthy controls) participated in this study. Complement protein levels were measured using enzyme-linked immunosorbent assay (ELISA) from serum samples. The severity of ASD symptoms was assessed using standardized diagnostic tools, including the Childhood Autism Rating Scale (CARS), the Autism Behavior Checklist (ABC), and Repetitive Behavior Scale-Revised (RBS-R). Serum C1q levels were significantly lower in the ASD group (p < 0. 001). C3 levels were lower (p = 0. 033), while C2 levels were slightly higher (p = 0. 015) in the ASD group. There are no significant differences in C4, MBL, or L-Ficolin levels. Logistic regression analysis identified reduced C1q levels as a significant predictor of ASD (p = 0. 001). However, this study found no significant correlations between complement levels and ASD symptom severity scores. The findings suggest that alterations in complement system proteins, particularly reduced serum C1q levels, may be associated with ASD. Given C1q's critical role in synaptic pruning and neuroimmune regulation, these results support the hypothesis that complement system dysfunction may contribute to the pathophysiology of ASD.

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