title: Proton magnetic resonance spectroscopy in subjects with high genetic risk of schizophrenia: investigation of anterior cingulate, dorsolateral prefrontal cortex and thalamus.
abstract: OBJECTIVE
  Reduced N-acetylaspartate levels in regions of the frontal cortex, including the anterior cingulate cortex, dorsolateral prefrontal cortex, and thalamus, involved in the pathophysiology of schizophrenia suggest that brain metabolite abnormalities may be a marker of genetic vulnerability to schizophrenia. We used proton magnetic resonance spectroscopy (H-MRS) to acquire absolute concentrations of brain metabolites in subjects with a high genetic risk of schizophrenia to investigate the potential relationship between unexpressed genetic liability to schizophrenia and neuronal dysfunction.
  
  
  METHODS
  Included in the study were 22 subjects who had at least two relatives with schizophrenia (high genetic risk group) and 22 controls with no second-degree relatives with schizophrenia. Absolute concentrations of N-acetylaspartate, creatine, choline, glutamate/glutamine, and myo-inositol and the ratios of metabolites in the anterior cingulate cortex, left dorsolateral prefrontal cortex, and left thalamus were measured using H-MRS at 1.5 Tesla.
  
  
  RESULTS
  Relative to the controls, the high genetic risk group showed significant differences in absolute metabolite levels in the spectra of the regions of the left thalamus, including significant decreases in N-acetylaspartate, creatine, and choline concentrations.
  
  
  CONCLUSIONS
  The study points to neuronal dysfunction, and in particular thalamic dysfunction, as a key region of the vulnerability marker of schizophrenia. Further studies should examine the nature of the thalamus more intensively to further our understanding of thalamic dysfunction as a vulnerability marker.
authors.affiliation: Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors.forename: So Young
authors.initials: SY
authors.lastname: Yoo
authors.forename: Suran
authors.initials: S
authors.lastname: Yeon
authors.forename: Chi-Hoon
authors.initials: CH
authors.lastname: Choi
authors.forename: Do-Hyung
authors.initials: DH
authors.lastname: Kang
authors.forename: Jong-Min
authors.initials: JM
authors.lastname: Lee
authors.forename: Na Young
authors.initials: NY
authors.lastname: Shin
authors.forename: Wi Hoon
authors.initials: WH
authors.lastname: Jung
authors.forename: Jung-Seok
authors.initials: JS
authors.lastname: Choi
authors.forename: Dong-Pyo
authors.initials: DP
authors.lastname: Jang
authors.forename: Jun Soo
authors.initials: JS
authors.lastname: Kwon
mesh_terms: D000293:Adolescent; D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D001931:Brain Mapping; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D005260:Female; D006179:Gyrus Cinguli / Q000378:metabolism*; D006801:Humans; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D017397:Prefrontal Cortex / Q000378:metabolism*; D011522:Protons; D011569:Psychiatric Status Rating Scales; D012559:Schizophrenia / Q000175:diagnosis* / Q000235:genetics* / Q000473:pathology; D013788:Thalamus / Q000378:metabolism*; D055815:Young Adult
chemical_list: D011522:Protons; D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline