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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