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Abstract #0839

Genetic association with prefrontal glutathione deficit: a preliminary 3T 1 H MRS study in early psychosis

Lijing Xin 1,2 , Ralf Mekle 3 , Carina Ferrari 1,4 , Philipp S. Baumann 1,4 , Luis Alameda 1,4 , Helene Moser 1 , Margot Fournier 1,4 , Huanxiang Lu 5 , Philippe Conus 4,6 , Rolf Gruetter 2,7 , and Kim Do 1,4

1 Unit for Research in Schizophrenia, Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital (CHUV), Lausanne, Switzerland, 2 Laboratory of Functional and Metabolic Imaging, Ecole Polytechnique Fdrale de Lausanne, Lausanne, Vaud, Switzerland, 3 Medical Physics, Physikalisch-Technische Bundesanstalt, Berlin, Germany, 4 National Center of Competence in Research (NCCR) SYNAPSY - The Synaptic Bases of Mental Diseases, Lausanne, Switzerland, 5 Institute of Surgical Technology and Biomechanics, University of Bern, Bern, Switzerland, 6 Service of General Psychiatry, Department of Psychiatry, Lausanne University Hospital (CHUV), Lausanne, Switzerland, 7 Departments of Radiology, University of Geneva, Geneva, Switzerland

Impairment of glutathione (GSH) metabolism has been reported in schizophrenia patients. Moreover, the GAG trinucleotide repeat (TNR) polymorphisms in the gene coding for the catalytic (GCLC) subunit of the glutamate-cysteine ligase (GCL), the rate-limiting enzyme for GSH synthesis, are associated with schizophrenia in case-control studies. The present study measured GSH levels in the medial prefrontal cortex of patients in early phase of psychosis and controls using short TE MRS at 3T and showed for the first time that the GAG-TNR high-risk genotype of the GCLC gene predicts lower prefrontal GSH levels in vivo.

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