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Analysis of selected studies suggests that interventions targeting the purinergic system, inflammation, and vitamin metabolism can yield measurable behavioral benefits in models of ASD

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The redox imbalance that results from combined glutathione depletion and increased ROS rapidly promotes phosphorylation and activation of the c-Jun N-terminal kinases (JNK) 1/2 [17,18], which translocate to mitochondria and further reduce mitochondrial respiration via SHP1-mediated inhibition of Src [19,20]