MR spectroscopic evaluation of N-acetylaspartate's T2 relaxation time and concentration corroborates white matter abnormalities in schizophrenia.
Magnetic resonance spectroscopy enables the in vivo analysis of certain aspects of brain biochemistry. Reduced N-acetylaspartate in key regions of schizophrenia has been reported repeatedly but not without controversy. Our objective is to investigate whether reduced N-acetylaspartate concentrations determined without correction for individual T2 relaxation time (referred to as 'apparent tNAA concentration') are due to a reduced absolute N-acetylaspartate concentration or to altered relaxation properties. For this purpose we measured absolute concentrations while evaluating individual T2 relaxation times. We evaluated the metabolite concentrations and metabolite/water relaxation times of a frontal white matter voxel from 23 patients who met DSM-IV criteria for schizophrenia and 29 healthy control subjects with similar age at a 3 T magnetic resonance scanner. A significantly reduced N-acetylaspartate concentration as well as shortened N-acetylaspartate's T2 relaxation time in the schizophrenic patient group was found. The apparent N-acetylaspartate concentration difference between healthy controls and patients with schizophrenia increased with the echo time due to a decreased N-acetylaspartate's T2 in the schizophrenic group. No group difference was found for any other metabolite concentration or metabolite/brain water relaxation time. These findings of reduced N-acetylaspartate as well as shortened N-acetylaspartate's T2 relaxation time give further evidence for microstructural white matter changes in schizophrenia. Furthermore, they elucidate why reports of a reduced N-acetylaspartate concentration in schizophrenia were not always corroborated.
Tunc-Skarka
Nuran
N
Department of Neuroimaging, Central Institute of Mental Health, Mannheim, Germany. nuran.tunc-skarka@zi-mannheim.de
Weber-Fahr
Wolfgang
W
Hoerst
Mareen
M
Meyer-Lindenberg
Andreas
A
Zink
Mathias
M
Ende
Gabriele
G
D000328:Adult; D000704:Analysis of Variance; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D004151:Dipeptides / Q000378:metabolism; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism* / Q000473:pathology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D009413:Nerve Fibers, Myelinated / Q000378:metabolism* / Q000473:pathology; D010725:Phosphocreatine / Q000378:metabolism; D011522:Protons; D012559:Schizophrenia / Q000378:metabolism / Q000473:pathology*; D014867:Water / Q000378:metabolism
D004151:Dipeptides; D011522:Protons; D010725:Phosphocreatine; D014867:Water; C027172:isospaglumic acid; D001224:Aspartic Acid; D018698:Glutamic Acid; C000179:N-acetylaspartate; D003401:Creatine