統合失調症の発達障害仮説と必須脂肪酸の関連についての考察
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概要
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Deficits in prepulse inhibition (PPI) are a biological marker for schizophrenia. To unravel the mechanisms that control PPI, we performed quantitative trait loci (QTL) analysis, on 1010 F2 mice derived by crossing C57BL/6 (B6) animals that show high PPI with C3H/He (C3) animals that show low PPI. We detected 6 major loci for PPI. A promising candidate on the chromosome 10-QTL was <I>Fabp7</I> (fatty acid binding protein 7, brain), a gene with functional links to the NMDA receptor and expression in neural stem/progenitor cells in developmental stage. <I>Fabp7</I>-deficient mice indeed showed decreased PPI. A quantitative complementation test supported <I>Fabp7</I> as a potential PPI-QTL gene. Disruption of <I>Fabp7</I> attenuated neurogenesis in vivo. Human <I>Fabp7</I> showed genetic association with schizophrenia. FABP7 is known to have high affinity for polyunsaturated fatty acids, in particular docosahexaenoic acid. These results suggest that FABP7 plays a novel and crucial role, linking the NMDA, neurodevelopmental and nutritional issues of schizophrenia pathology.
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