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Genetic imprinting in schizophrenia



Genetic imprinting in schizophrenia



Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 706 15



A growing body of evidence suggests that the 5HT2A receptor (5HT2AR) may play a role in the aetiology and treatment of psychiatric disorders. Some but not all of the numerous 5HT2AR studies have reported association between schizophrenia and the silent 5HT2A 102 T/C genetic polymorphism. Epigenetic factors, such as RNA splicing, RNA editing and genetic imprinting, may be responsible for some of these contradictory findings and these factors can have marked effects on phenotypic variation. We are testing the hypothesis that polymorphic imprinting of the 5HT2AR gene1 and also of other gene candidates, such as 5HT2CR and COMT, may be frequent enough to confound current genetic paradigms.) Initially expression of the 5HT2AR T102 and C102 alleles in the prefrontal cortex of schizophrenia cases (n=10) and normal controls (n=8) have been compared. All subjects were heterozygous for this polymorphism. When the ratios of expression levels of each allele (T/C) were compared between the patient and control groups, no significant differences were detected. However, one individual with schizophrenia exhibited complete imprinting of the C102 allele. A previous study in 18 controls reported 4 individuals with complete imprinting using this marker1, indicating that 5HT2AR gene imprinting is highly variable. Studies of 5HT2C and COMT are ongoing. These preliminary findings demonstrate that interpretations based solely on the genotype of subjects would be misleading, and that gene expression levels should also be considered.)1. Bunzel R, Blumcke I, Cichon S et al. Mol Brain Res 1998; 59, 90-92.

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