title: Negative correlation between brain glutathione level and negative symptoms in schizophrenia: a 3T 1H-MRS study.
abstract: BACKGROUND
  Glutathione (GSH), a major intracellular antioxidant, plays a role in NMDA receptor-mediated neurotransmission, which is involved in the pathophysiology of schizophrenia. In the present study, we aimed to investigate whether GSH levels are altered in the posterior medial frontal cortex of schizophrenic patients. Furthermore, we examined correlations between GSH levels and clinical variables in patients.
  
  
  RESULTS
  Twenty schizophrenia patients and 16 age- and gender-matched normal controls were enrolled to examine the levels of GSH in the posterior medial frontal cortex by using 3T SIGNA EXCITE (1)H-MRS with the spectral editing technique, MEGA-PRESS. Clinical variables of patients were assessed by the Global Assessment of Functioning (GAF), Scale for the Assessment of Negative Symptoms (SANS), Brief Psychiatric Rating Scale (BPRS), Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS), and five cognitive performance tests (Word Fluency Test, Stroop Test, Trail Making Test, Wisconsin Card Sorting Test and Digit Span Distractibility Test). Levels of GSH in the posterior medial frontal cortex of schizophrenic patients were not different from those of normal controls. However, we found a significant negative correlation between GSH levels and the severity of negative symptoms (SANS total score and negative symptom subscore on BPRS) in patients. There were no correlations between brain GSH levels and scores on any cognitive performance test except Trail Making Test part A.
  
  
  CONCLUSIONS
  These results suggest that GSH levels in the posterior medial frontal cortex may be related to negative symptoms in schizophrenic patients. Therefore, agents that increase GSH levels in the brain could be potential therapeutic drugs for negative symptoms in schizophrenia.
authors.affiliation: Department of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Matsuzawa
authors.forename: Takayuki
authors.initials: T
authors.lastname: Obata
authors.forename: Yukihiko
authors.initials: Y
authors.lastname: Shirayama
authors.forename: Hiroi
authors.initials: H
authors.lastname: Nonaka
authors.forename: Yoko
authors.initials: Y
authors.lastname: Kanazawa
authors.forename: Eiji
authors.initials: E
authors.lastname: Yoshitome
authors.forename: Junichi
authors.initials: J
authors.lastname: Takanashi
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Matsuda
authors.forename: Eiji
authors.initials: E
authors.lastname: Shimizu
authors.forename: Hiroo
authors.initials: H
authors.lastname: Ikehira
authors.forename: Masaomi
authors.initials: M
authors.lastname: Iyo
authors.forename: Kenji
authors.initials: K
authors.lastname: Hashimoto
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D016022:Case-Control Studies; D003071:Cognition; D005260:Female; D005838:Genotype; D005978:Glutathione / Q000378:metabolism*; D006801:Humans; D009682:Magnetic Resonance Spectroscopy / Q000379:methods*; D008297:Male; D018384:Oxidative Stress; D017397:Prefrontal Cortex / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D012559:Schizophrenia / Q000378:metabolism* / Q000473:pathology
chemical_list: D000975:Antioxidants; D016194:Receptors, N-Methyl-D-Aspartate; D005978:Glutathione