ArticleMetabolic brain disease2026
Environmental metals, prostaglandin pathways, and immune-mediated neuroinflammation in autism spectrum disorder: A secondary analysis of peripheral biomarker studies.
Article in Metabolic brain disease, 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
Autism spectrum disorder (ASD) shows peripheral signatures of inflammation, cellular stress, and immune dysregulation in subsets of affected children. This secondary analysis synthesized four published cross-sectional biomarker studies to describe group differences and develop an organizing, exposure-linked working model consistent with reported clinical features. For studies reporting parametric statistics, published means and standard deviations were abstracted to compute within-study standardized mean differences with 95% confidence intervals. For nonparametric results, medians, interquartile ranges, and proportions above thresholds were reported as published. In the prostaglandin-focused study, ASD showed very large between-group differences in prostaglandin E₂ and its synthetic pathway markers, including cyclooxygenase-2 and microsomal prostaglandin E synthase-1, alongside higher nuclear factor κB and lower EP₂ receptor measures. In the separate study of regulatory and stress markers, heat shock protein 70 was higher, and hematopoietic prostaglandin D₂ synthase was lower, while transforming growth factor-β2 changes were modest and imprecise. In metal-focused studies, blood lead and mercury levels were elevated in individuals with ASD. They were reported alongside anti-ribosomal P protein autoantibodies and neurokinin A, respectively, and were associated with ASD severity indices and sensory features. These peripheral patterns support a testable hypothesis that toxic metal burden, redox-sensitive inflammatory signaling, and prostaglandin-pathway activation converge in biomarker-defined ASD subgroups. All biomarkers analyzed were measured in blood-based matrices (plasma, serum, or whole blood) and are interpreted as peripheral signatures that may intersect with neuroimmune mechanisms under permissive conditions rather than as direct evidence of central nervous system neuroinflammation or brain-directed autoimmunity.
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