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glutathione psychosis deficiency in the early postnatal developmental period as a neurodevelopmental animal model of schizophrenia | Pharmacological Reports Potential pathways involved in the

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These symptoms are more likely linked to the underlying condition causing the elevated B12 levels, rather than the high B12 levels themselves 17

glutathione psychosis deficiency in the early postnatal developmental period as a neurodevelopmental animal model of schizophrenia | Pharmacological Reports Potential pathways involved in the

As no significant differences in serum homocysteine, cystathionine (Figures 4 and 5) or serine levels [60, 69, 70, 75] were observed in children with autistic disorder compared to those without, it can be inferred that the low levels of cysteine may be caused by decreased cystathione lyase activity and/or increased utilisation of sulphate and/or taurine and/or lower dietary intake or absorption of cysteine in children with autistic disorder

glutathione psychosis deficiency in the early postnatal developmental period as a neurodevelopmental animal model of schizophrenia | Pharmacological Reports Potential pathways involved in the

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glutathione psychosis deficiency in the early postnatal developmental period as a neurodevelopmental animal model of schizophrenia | Pharmacological Reports Potential pathways involved in the

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glutathione psychosis deficiency in the early postnatal developmental period as a neurodevelopmental animal model of schizophrenia | Pharmacological Reports Potential pathways involved in the

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