ArticleFrontiers in psychiatry2026
Anti-GAD antibody biochemical correlates of autism symptoms in children: a case-control study.
Article in Frontiers in psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: To evaluate whether anti-glutamic acid decarboxylase (Anti-GAD) antibodies and selected biochemical parameters are associated with autism spectrum disorder (ASD), symptom severity, and autistic regression in a case-control design. We hypothesized that Anti-GAD titers would be higher in ASD and associated with greater symptom burden. Materials and Methods: Children aged 2-9 years with ASD diagnosed according to DSM-5 criteria and age- and sex-matched healthy controls were included. Laboratory analyses assessed Anti-GAD, ASO, ferritin, iron, vitamin D, vitamin B12, thyroid-stimulating hormone, and folate. Clinical evaluations included the Autism Behavior Checklist (ABC), Modified Checklist for Autism in Toddlers (M-CHAT), and Ankara Developmental Screening Inventory (AGTE). Autistic regression was defined as loss of previously acquired language and/or social communication skills lasting ≥3 months between 15 and 30 months of age. Results: Ninety children participated (45 with ASD and 45 controls). Anti-GAD antibody levels were higher in the ASD group than in controls (p = 0.003). Although statistically significant, the absolute difference between groups was modest. Among ASD cases, 62% met criteria for regression; this relatively high proportion may reflect the clinic-based sampling and the operational definition applied. Compared with those without regression, children with regression had higher Anti-GAD titers and ABC scores but lower iron and ferritin levels (all p < 0.05). Anti-GAD levels correlated positively with ABC total scores (r = 0.724, p = 0.01). These findings reflect statistical associations and do not imply causality. Conclusion: Higher Anti-GAD antibody levels were statistically associated with ASD, autistic regression, and greater behavioral symptom severity in this sample. These results suggest possible immune-related contributions to ASD heterogeneity; however, larger longitudinal studies are needed before clinical or biomarker implications can be established.
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