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As an example, a recent paper by Rossignol and Frye reviewed the literature on inflammation and its relationship to autism but never mentioned excitotoxicity or GluRs dysfunction.[206] Most of the autism literature tends to follow this pattern.[24,41,108,164] Yet, a growing literature strongly suggest a link to abnormalities in glutamate and/or GluR function as major players in ASDs, which includes children, high functioning autism, and adults with autism.[80,223,224,282] The ability of immune cytokines and other immune mediators of inflammation, to enhance microglial priming/activation and to magnify the excitotoxic potential of GluRs, indicate that the two processes operate together, both physiologically and pathologically

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Biochemically, cells present with depletion of intracellular glutathione and subsequent decreased activity of GPX4