Schizophrenia is a debilitating mental disorder that afflicts about 1% of the population worldwide. Despite intensive, multifaceted research, its exact etiology remains elusive. Epidemiological data shows that when pregnant mothers experienced malnutrition or famine (e.g. the Dutch Hunger Winter of 1994-1945 and the Chinese famine of 1959-1961), the risk of schizophrenia in their children increased by two fold. This fact could be considered in the context of Developmental Origins of Health and Disease (DOHaD) or fetal programming. The concept of DOHaD is well referenced in the understanding of adult metabolic diseases, but less so in the field of mental disorders. We will attempt to show how the mechanisms of DOHaD could contribute at least in part to schizophrenia pathogenesis. Resonating with this concept, we introduce mainly our data showing increased expression of genes for fatty acid binding proteins (FABPs) in the postmortem brains from patients with schizophrenia and the beneficial effect conferred by the administration of polyunsaturated fatty acids (PUFAs) during the early developmental period of rats.
Keywords: Endophenotype, prepulse inhibition, FABP7, genetic association, postmortem brain, gene expression
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