AbstractPhospholipids and related molecules make up around 60% of the dry weight of the brain and an even higher proportion of synapses and synaptic vesicles. They influence the quaternary structure of all membrane-associated proteins and play important signal transduction roles following activation of most known neuronal receptors for transmitters, cytokines and growth factors. There is now substantial evidence that phospholipid composition and oxidation are altered at the onset of schizophrenic illness and therefore that these alterations may possibly play a causative role. Large numbers of enzymes, enzyme-regulatory factors and transport proteins are involved in the synthesis, turnover and degradation of brain phospholipids. The chromosomal locations of many of these proteins are known and it is of interest to relate these to chromosomal locations which have been identified as possible sites for genes involved in schizophrenia. A detailed tabulation of these locations has been published (Prostaglandins Leukotrienes EFAS 2000; 63: 47-59). Sites of particular interest are those for phospholipase A2 and Apo-AII on chromosome 1, Apo B on chromosome 2, fatty acid binding protein (FABP)-2 on chromosome 4, prostaglandin E (PGE) receptor-2, leukotriene-4 synthase and FABP-6 on chromosome 5, various phospholipid-related enzymes and FABP7 on chromosome 6, fatty acid transport protein on chromosome 7, various phospholipid and prostaglandin-related enzymes on chromosome 9, Apo AI, IV and CIII on chromosome 11, FLAP on chromosome 13, LCAT on chromosome 16, various phospholipases on chromosome 20 and FACL4 on chromosome X.
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