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Redox homeostasis disruption is responsible for synaptic dysfunction, neuroinflammation, and disrupted neuronal signaling, worsening the fundamental symptoms of ASD

In addition to 0.6mmol/l HepG2 ATP7B-KO cells, 0.2mmol/l HepG2 ATP7B-KO cells presented increased levels of these four markers

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Patients with stable schizophrenia had significantly lower scores on the ACC glutathioneglutamate component, an effect almost entirely leveraged by the sub-group of patients with residual schizophrenia