1. N-Acetylaspartylglutamate (NAAG) and N-Acetylaspartate (NAA) in Patients With Schizophrenia
- Author
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Frank Träber, H. H. Schild, Kai-Uwe Kühn, Nadine Petrovsky, Natascha Fingerhut, Alois M. Sprinkart, Wolfgang Block, Michael Wagner, Frank Jessen, and Wolfgang Maier
- Subjects
Adult ,instrumentation [Magnetic Resonance Spectroscopy] ,Male ,medicine.medical_specialty ,Magnetic Resonance Spectroscopy ,metabolism [Prefrontal Cortex] ,Prefrontal Cortex ,Neuropsychological Tests ,Functional Laterality ,N-acetylaspartate ,Internal medicine ,mental disorders ,medicine ,Humans ,In patient ,ddc:610 ,Effects of sleep deprivation on cognitive performance ,physiopathology [Prefrontal Cortex] ,Prefrontal cortex ,analogs & derivatives [Aspartic Acid] ,Psychiatric Status Rating Scales ,isospaglumic acid ,Aspartic Acid ,Positive and Negative Syndrome Scale ,metabolism [Dipeptides] ,physiology [Functional Laterality] ,Regular Article ,Dipeptides ,medicine.disease ,metabolism [Aspartic Acid] ,Cortex (botany) ,methods [Magnetic Resonance Spectroscopy] ,Psychiatry and Mental health ,Endocrinology ,nervous system ,Frontal lobe ,Schizophrenia ,Female ,metabolism [Schizophrenia] ,physiopathology [Schizophrenia] ,Protons ,Psychology ,Neuroscience - 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.
- Published
- 2011
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