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Converging evidence highlights mitochondrial dysfunction and oxidative stress, resulting from excessive production of reactive oxygen species (ROS) and/or insufficient antioxidant defenses, in both peripheral tissues and brain samples of individuals with ASD (Lin et al., 2022) This oxidative dysregulation is thought to exacerbate neuroinflammation, mitochondrial dysfunction, and synaptic abnormalities, which may underlie some of the core behavioral and cognitive impairments seen in ASD (Gevezova et al., 2023)