Abstract
Schizophrenia is a major mental disorder with no clearly identified pathophysiology. A variety of theories has been proposed to explain the pathophysiology of schizophrenia. One approach that is finding empirical support is the investigation of membrane composition and function. Evidence to date suggests that there are defects in phospholipid metabolism and cell signaling in schizophrenia. Specifically, low levels of arachidonic acid (AA)–enriched phospholipids have been observed in both central and peripheral tissues. It is well known that changes in membrane composition are associated with a variety of functional consequences. Since AA has many key roles in neural functioning, understanding its significance for the pathophysiology of schizophrenia may lead to novel approaches to improving treatment of schizophrenia. The purpose of this review is thus to explore some of the roles of AA signaling in biological, physiological, and clinical phenomena observed in schizophrenia.
Highlights
Research over the last century has suggested that neuronal maldevelopment, impaired neurotransmission, intrauterine viral infections, autoimmune dysfunction, and many other mechanisms may underlie the pathophysiology of schizophrenia
The accelerated breakdown of membrane phospholipids is indirectly supported by the 31P Magnetic Resonance Spectroscopy (31P MRS) findings as well as direct measurements of phospholipid fatty acids in the brains of schizophrenic patients
We have demonstrated that drug-free schizophrenic patients exhibit reduced physiologic responsivity mediated through the platelet 5-HT2 receptor complex, which can be modified by haloperidol treatment[43]
Summary
There are a large variety of seemingly disparate biological findings[1], possibly due to etiologic heterogeneity. This would suggest that there are one or more (but very few) common pathogenetic pathways that lead to the syndromes of schizophrenia. Alterations in AA are associated with membrane dysfunction of clinical relevance. This defect appears to be independent of neuroleptic treatment (based on findings from drug free and neuroleptic-naive patients), and is associated with illness severity. Supplementation with essential fatty acids (EFA) is associated with increased membrane PUFAs and with improved clinical state
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