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Volume 81, Issue 5, Pages 307-308 (November 2009)


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A human in vivo study of the extent to which 31-phosphorus neurospectroscopy phosphomonoesters index cerebral cell membrane phospholipid anabolism

B.K. PuriaCorresponding Author Informationemail address, I.H. Treasadenb

published online 11 November 2009.

Abstract 

The phosphomonoester narrow resonance of human in vivo 31-phosphorus neurospectroscopy studies is believed to index the anabolism of cell membrane phospholipids and has therefore been used to study phospholipid anabolism in the brain non-invasively. However, it is an indirect measure of phospholipid metabolism and although it does contain major contributions from phosphocholine, phosphoethanolamine and L-phosphoserine, which are important precursors of membrane phospholipids, many other metabolites, including sugar phosphates, can contribute to this region of the spectrum, and separation of these different peaks is not achieved with the present in vivo methodology. Recently, it has become possible to analyze signal directly from the cell membrane motion-restricted phospholipids by analysis of a broad resonance signal. We therefore hypothesized that there should be a positive correlation between the phosphomonoester narrow resonance and the broad resonance signal if the former does indeed index cell membrane phospholipid anabolism. Cerebral 31-phosphorus magnetic resonance spectroscopy was carried out in 54 human subjects, including normal volunteers and patients with schizophrenia in order to widen the range of phosphomonoester and broad resonance values. Spectra were obtained from 70×70×70mm3 voxels using an image-selected in vivo spectroscopy pulse sequence. There was a highly significant positive correlation between the phosphomonoester resonances and the broad resonance signals (r=0.404, P<0.005). These results are consistent with the hypothesis that the phosphomonoester narrow resonance does indeed index cell membrane phospholipid anabolism in brain studies.

a MRI Unit, Imaging Sciences Department, MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London W12 0HS, England, UK

b Three Bridges Medium Secure Unit, West London Mental Health NHS Trust, Uxbridge Road, Middlesex UB1 3EU and Head of Forensic Neurosciences, Lipid Neuroscience Group, Imperial College London, England, UK

Corresponding Author InformationCorresponding author. Tel.: +442083832412; fax: +442083833038.

PII: S0952-3278(09)00173-2

doi:10.1016/j.plefa.2009.10.003


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