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Tony P. George, MD
Department of Psychiatry Yale University School of Medicine Neuropsychopharmacology Research Unit, Room B-254 Sterling Hall of Medicine 333 Cedar St New Haven, CT 06520-8066

Matthew W. Spence, MD, PhD
Alberta Heritage Foundation for Medical Research Edmonton, Alberta

Arch Gen Psychiatry. 1996;53(11):1065-1066.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Stanley et al¹ used phosphorus 31 magnetic resonance spectroscopy to evaluate high-energy phosphate metabolism in the prefrontal cortex of patients with schizophrenia and control subjects. Stanley et al and Pettegrew et al² have documented changes in the membrane phospholipid metabolism of patients with schizophrenia, and they have suggested that these changes may, in part, be involved in the pathophysiology of schizophrenic illnesses. They found that the levels of phosphomonoesters (PMEs) (ie, the precursors of phospholipid biosynthesis) and orthophosphates were reduced and that the levels of phosphodiesters (PDEs) (ie, phospholipid degradation products) and intracellular magnesium were elevated in the prefrontal cortex of patients with schizophrenia who were and were not taking medication. They suggested that the reduction of PMEs could be due to the decreased biosynthesis or the altered degradation of PMEs and that the increase of PDEs may be due to the increase of phospholipase A₁ . . . [Full Text PDF of this Article]

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