31P NMR spectroscopy of phospholipid metabolites in postmortem schizophrenic brain

✍ Scribed by Richard A. Komoroski; John M. Pearce; Robert E. Mrak

• Publisher: John Wiley and Sons
• Year: 2008
• Tongue: English
• Weight: 102 KB
• Volume: 59
• Category: Article
• ISSN: 0740-3194
• DOI: 10.1002/mrm.21516

✦ Synopsis

Abstract

Evidence has been accumulating that schizophrenia involves abnormalities in the composition and metabolism of cell membrane phospholipids (PLs) in the brain. In vivo ^31^P MRS has been used to measure the metabolic precursors and degradation products of PL metabolism in schizophrenia. Because in vivo line widths are substantially broader than in solution, only the broad phosphomonoester (PME) and phosphodiester bands, or partly resolved resonances of individual metabolites, are typically measured in vivo in the ^31^P spectrum. In addition to poor resolution, the relatively low signal‐to‐noise ratio (SNR) makes precise quantitation difficult. An alternative with substantially better resolution and precision for quantitation is high‐resolution NMR spectroscopy of extracts of samples from postmortem brain. Here we determine absolute concentrations of the individual PL metabolites phosphocholine (pc), phosphoethanolamine (pe), glycerophosphocholine (gpc), and glycerophosphoethanolamine in aqueous extracts of tissue from frontal, temporal, and occipital cortex of postmortem brain for schizophrenics, controls, and patients with other mental illnesses (psychiatric controls [PC]) using high‐resolution ^31^P NMR spectroscopy. For the complete groups, which included both males and females, there were no statistically significant differences for schizophrenics vs. controls for any of the four PL metabolites in any of the three brain regions. Trends (0.05 < P < 0.10) were noted for increased gpc in schizophrenia in all three regions. PC differed from both controls and schizophrenics in several measures. When only males were considered, gpc was significantly (P < 0.05) elevated in all three brain regions in schizophrenia. Magn Reson Med 59:469–474, 2008. © 2008 Wiley‐Liss, Inc.