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Schizophrenia: glutathione deficit in cerebrospinal fluid and prefrontal cortex in vivo
European Journal of Neuroscience
DA - 20001103 IS - 0953-816X LA - eng PT - Journal Article RN - 0 (Reactive Oxygen Species) RN - 51-61-6 (Dopamine) RN - 70-18-8 (Glutathione) SB - IM Institution : Brain Research Institute, University of Zurich and Centre for Research in Psychiatric Neuroscience, University of Lausanne, Route de Cery, CH-1008 Prilly-Lausanne, Switzerland. Kim.Do@inst.hospvd.ch Mention de responsabiblité : Do,K.Q.;Trabesinger,A.H.;Kirsten-Kruger,M.;Lauer,C.J.;Dydak,U.;Hell,D.;Holsboer,F.;Boesiger,P.;Cuenod,M. SAPHIRID:48100
Schizophrenia is a major psychiatric disease, which affects the centre of the personality, with severe problems of perception, cognition as well as affective and social behaviour. In cerebrospinal fluid of drug-free schizophrenic patients, a significant decrease in the level of total glutathione (GSH) by 27% (P<0.05) was observed as compared to controls, in keeping with the reported reduced level of its metabolite gamma-glutamylglutamine. With a new non-invasive proton magnetic resonance spectroscopy methodology, GSH level in medial prefrontal cortex of schizophrenic patients was found to be 52% (P = 0.0012) lower than in controls. GSH plays a fundamental role in protecting cells from damage by reactive oxygen species generated among others by the metabolism of dopamine. A deficit in GSH would lead to degenerative processes in the surrounding of dopaminergic terminals resulting in loss of connectivity. GSH also potentiates the N-methyl-D-aspartate (NMDA) receptor response to glutamate, an effect presumably reduced by a GSH deficit, leading to a situation similar to the application of phencyclidine (PCP). Thus, a GSH hypothesis might integrate many established biological aspects of schizophrenia
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