title: N-acetylaspartylglutamate (NAAG) and N-acetylaspartate (NAA) in patients with schizophrenia.
abstract: BACKGROUND : Imbalance of glutamatergic neurotransmission has been proposed as a key mechanism underlying symptoms of schizophrenia. The neuropetide N-acetylaspartylglutamate (NAAG) modulates glutamate release. NAAG provides a component of the proton magnetic resonance spectrum (1H-MRS) in humans. The signal of NAAG, however, largely overlaps with its precursor and degrading product N-acetylaspartate (NAA) that by itself does not act in glutamatergic neurotransmission.
  
  
  METHODS
  We quantified NAAG and NAA separately from the 1H-MRS signal in 20 patients with schizophrenia and 20 healthy comparison subjects on a 3.0 Tesla MR scanner. The 1H-MRS voxels were positioned in the anterior cingulate cortex (ACC) and in the left frontal lobe. Psychopathological symptoms and cognitive performance were assessed.
  
  
  RESULTS
  In the ACC, the ratio NAAG/NAA was increased (P = .041) and NAAG was increased at a trend level (P = .066) in patients, while NAA was reduced (P = .030). NAA correlated with attention performance in patients (r = .64, P = .005) in the ACC. There was no group difference of NAAG, NAA, or NAAG/NAA in the frontal lobe but an inverse correlation of NAAG with negatives symptoms (Positive and Negative Symptoms Scale [PANSS] negative, r = -.58, P = .018) and with the total symptom score (PANSS total, r = -.50, P = .049). In addition, there was a positive correlation of frontal lobe NAAG (r = .53, P = .035) and NAAG/NAA (r = .54, P = .030) with episodic memory in patients.
  
  
  CONCLUSIONS
  In this study, we present the first in vivo evidence for altered NAAG concentration in patients with schizophrenia.
authors.affiliation: Department of Psychiatry and Psychotherapy, University of Bonn, Germany. frank.jessen@ukb.uni-bonn.de
authors.forename: Frank
authors.initials: F
authors.lastname: Jessen
authors.forename: Natascha
authors.initials: N
authors.lastname: Fingerhut
authors.forename: Alois M
authors.initials: AM
authors.lastname: Sprinkart
authors.forename: Kai-Uwe
authors.initials: KU
authors.lastname: Kühn
authors.forename: Nadine
authors.initials: N
authors.lastname: Petrovsky
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Maier
authors.forename: Hans-H
authors.initials: HH
authors.lastname: Schild
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Block
authors.forename: Michael
authors.initials: M
authors.lastname: Wagner
authors.forename: Frank
authors.initials: F
authors.lastname: Träber
mesh_terms: D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D004151:Dipeptides / Q000378:metabolism*; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D009682:Magnetic Resonance Spectroscopy / Q000295:instrumentation / Q000379:methods*; D008297:Male; D009483:Neuropsychological Tests; D017397:Prefrontal Cortex / Q000378:metabolism* / Q000503:physiopathology; D011522:Protons; D011569:Psychiatric Status Rating Scales; D012559:Schizophrenia / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D004151:Dipeptides; D011522:Protons; C027172:isospaglumic acid; D001224:Aspartic Acid; C000179:N-acetylaspartate