ArticleFrontiers in immunology2026
Early-life oxidative stress programs persistent NFκB activation and neuroinflammation in autism spectrum disorder.
Article in Frontiers in immunology, 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
Background: Oxidative stress and immune dysregulation are hallmark features of autism spectrum disorder (ASD), yet whether oxidative imbalance acts as an upstream trigger of immune activation remains unclear. The redox-sensitive transcription factor NFκB represents a potential mechanistic link. We investigated whether early-life oxidative stress contributes to persistent NFκB activation and neuroinflammation in ASD. Methods: Umbilical cord blood and peripheral blood from ASD and typically developing children were analyzed for redox markers (GSH/GSSG ratio, malondialdehyde, 8-oxo-dG), NFκB activation (p65 DNA-binding and nuclear translocation), and inflammatory gene expression. The mechanistic relationship between oxidative stress and NFκB signaling was investigated in prenatal valproic acid (VPA)-exposed mice using antioxidant intervention (N-acetylcysteine, NAC), NFκB inhibition (Bay 11-7082), pro-oxidant challenge, behavioral assays, and primary amygdala neuron models. Results: ASD children exhibited persistent oxidative imbalance detectable at birth, accompanied by increased NFκB activation and pro-inflammatory gene expression. VPA-exposed mice recapitulated these molecular and behavioral abnormalities. In primary neurons, oxidative stress directly enhanced NFκB activity and promoter binding, whereas antioxidant and mitochondrial-targeted approaches suppressed NFκB activation. Developmentally, oxidative stress preceded sustained NFκB activation, and prenatal, but not postnatal, NAC treatment prevented these abnormalities. NAC restored redox homeostasis, reduced NFκB signaling, and improved behavioral deficits, whereas NFκB inhibition alone attenuated inflammatory responses but failed to correct oxidative imbalance or behavioral abnormalities. Conclusion: Early-life oxidative stress is an upstream pathogenic event associated with persistent NFκB activation and neuroinflammation in ASD. NFκB primarily mediates inflammatory signaling, while oxidative stress likely contributes to ASD-related behaviors through additional downstream pathways. These findings highlight early redox modulation as a potential therapeutic strategy.
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