There is evidence of abnormalities of prostaglandin synthesis and action in schizophrenia; thus, there are reports of increased activity of phospholipase A2,1 increased plasma levels of prostaglandin E2,2 and subsensitivity of platelet prostaglandin receptors.3 The main precursor for prostaglandin synthesis is arachidonic acid, which is released from membrane phospholipid by phospholipase A2. One possible consequence of increased phospholipase A2 activity would be the depletion of arachidonic acid.
In the course of a study of membrane fatty acids, we measured4 red blood cell membrane arachidonic acid in a group of 23 hospitalized neuroleptic-treated schizophrenic patients (16 men and 7 women) aged 28 to 75 years (mean age, 55 years) and 16 control subjects matched for age and sex. We also measured the plasma levels of thiobarbituric acid reactive substances (TBARS) in the same blood samples. Thiobarbituric acid reactive substances are a measure of
Peet M, Laugharne JDE, Horrobin DF, Reynolds GP. Arachidonic Acid: A Common Link in the Biology of Schizophrenia? Arch Gen Psychiatry. 1994;51(8):665–666. doi:10.1001/archpsyc.1994.03950080077012
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