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Consistent with previous studies, NFκB dysregulation contributes to ASD-associated neuroinflammation, including glial activation and inflammatory signaling, but likely acts within a broader pathological network rather than as a single causal mechanism ( Translational considerations and therapeutic implications of redox modulation in ASD Although our data support a mechanistic link between oxidative stress and NFκB-driven neuroinflammation, the translational implications remain preliminary
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