Indexation of cerebral cell membrane phospholipid catabolism by the non-invasively determined cerebral 31-phosphorus neurospectroscopic phosphodiester peak.

Breakdown of mammalian cerebral cell membrane phospholipids releases phosphorylated polar head groups from the sn-3 phospholipid position, including phosphorylcholine and phosphorylethanolamine. Glycerophosphorylcholine and glycerophosphorylethanolamine are on their catabolic pathways and have been assigned to the phosphodiester narrow resonance obtained from 31-phosphorus neurospectroscopy, accounting for approximately 38% of the overall signal; therefore in human in vivo 31-phosphorus neurospectroscopy neuropsychiatric studies this narrow resonance has been used to index the catabolism of cerebral cell membrane phospholipids non-invasively. However, for ethical reasons direct assessment of this assumption has not hitherto been possible in humans. Recently, it has become possible to analyze signal directly from the cell membrane motion-restricted phospholipids by analysis of a broad resonance signal. It was therefore hypothesized that there should be a negative correlation between the phosphodiester narrow resonance and the broad resonance signal if the former does indeed index cell membrane phospholipid catabolism. Cerebral 31-phosphorus magnetic resonance spectroscopy was carried out in 54 human subjects (mean age 38 years; 41 male), including normal volunteers and patients with schizophrenia, in order potentially to widen the range of phosphodiester and broad resonance values. Spectra were obtained from 70 × 70 × 70 mm(3) voxels using an image-selected in vivo spectroscopy pulse sequence. There was a highly significant negative correlation between the phosphodiester resonances and the broad resonance signals (r=-0.509, P<0.0001). This result is consistent with the hypothesis that the phosphodiester narrow resonance does index cell membrane phospholipid catabolism in non-invasive human neuropsychiatric studies.