Influence of gene on symptom severity of schizophrenia.

OBJECTIVE

Recent advances have provided compelling evidence for the role of excessive complement activity in the pathophysiology of schizophrenia. In this study, we aimed to detect the association of the gene encoding complement factor H (), a regulator in complement activation, with schizophrenia.

MATERIALS AND METHODS

A sample of 1783 individuals with or without schizophrenia was recruited for genetic analysis. Genomic DNA samples were extracted from peripheral blood cells using multiplex polymerase chain reaction and the SNaPshot assay. A Database for Schizophrenia Genetic Research (SZDB) was used to detect the association of brain expression with schizophrenia. Next, we performed a genotype-phenotype analysis to identify the relationship between Y402H polymorphism and clinical features of schizophrenia.

RESULTS

There was a significant association of hippocampal expression with schizophrenia (=0.017), whereas this significance did not survive after adjusting for false discovery rate (=0.105). Comparing the genotype and allele frequencies of the genotyped single-nucleotide polymorphisms between case and control groups showed no significant difference. There were significant differences in the scores of negative symptoms and delayed memory between the patients with C allele and those without C allele (<0.01 and =0.04 after Bonferroni correction, respectively). Furthermore, we observed a marginally significant association between the Y402H polymorphism and expression in the hippocampus (=0.051); however, this significance was lost after multiple testing correction (=0.51, after Bonferroni correction).

CONCLUSION

Our findings provide suggestive evidence for the role of in the development of negative symptoms and cognitive dysfunction in schizophrenia.