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Phospholipid composition of postmortem schizophrenic brain by 31 P NMR spectroscopy
Author(s) -
Pearce John M.,
Komoroski Richard A.,
Mrak Robert E.
Publication year - 2009
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.21820
Subject(s) - phospholipid , phosphatidylethanolamine , metabolite , nuclear magnetic resonance spectroscopy , chemistry , in vivo , medicine , biochemistry , biology , membrane , phosphatidylcholine , genetics , organic chemistry
Cell membrane abnormalities due to changes in phospholipid (PL) composition and metabolism have been implicated in schizophrenia pathogenesis. That work has generally assessed membrane phospholipids from nonneural tissues such as erythrocytes and platelets. High‐resolution 31 P NMR spectroscopy was used to characterize PLs of gray matter in postmortem brain for 20 schizophrenics, 20 controls, and 7 patients with other mental illnesses (psychiatric controls). Tissues from frontal, temporal, and occipital cortices were extracted with hexane–isopropanol, and 31 P NMR spectra were obtained in an organic–solvent system to resolve the major PL classes (based on headgroups) and subclasses (based on linkage at the sn − 1 position). Surprisingly, repeated‐measures multivariate analysis of variance revealed no overall differences among the groups. There were no significant differences ( P < .05) among the three groups for any individual PL subclass, including lysophospholipids. The sum of all phosphatidylethanolamine headgroups was significantly lower for schizophrenics than for controls or psychiatric controls in the frontal cortex. The present results are minimally correlated with previous results for aqueous PL metabolites on these same samples. The metabolite changes measured by in vivo 31 P MRS in schizophrenia do not appear to reflect PL concentration changes. The present results offer very little support for the phospholipid hypothesis of schizophrenia. Magn Reson Med 61:28–34, 2009. © 2008 Wiley‐Liss, Inc.

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