An Association Study Between The NCAM Gene And Schizophrenia

Based on evidence for a major contribution of genetic factors, decades of extensive efforts have been dedicated to the search of DNA sequence variations that increase the risk to SCZ. However, the mode of transmission is complex and non-Mendelian. Several factors such as possible involvement of numerous interactive genes of minor effect, yet unknown environmental effects and diagnostic ambiguities of the disease have made genetic studies in SCZ quite unproductive. However, in the last two years, because of the availability of the complete human genomic sequence, along with technology advances and cost reductions in SNP identification and genotyping and the coordination of genome-wide scans by world wide consortia, many promising chromosome regions now have support from multiple independent studies. With fine mapping in these regions, several research groups recently announced discovering of susceptibility genes of schizophrenia.We focus on NCAM which is a new susceptibility gene of schizophrenia. NCAM is a multifunction transmembrane protein involved in synaptic plasticity, neurodevelopment, and neurogenesis. In recently study, several lines of evidence suggest that NCAM is a compelling candidate gene for neurocognitive functioning in schizophrenia.Neurocognition is widely recognized as a highly plausible endophenotype for schizophrenia.As for NCAM, we report a result obtained from a case-control study in the Chinese population (288 schizophrenics, 288 controls). Five SNPs(rs1943620, rs1836796, rs1821693, rs686050, rs584427) of the NCAM gene that was reported by Sullivan et al. were genotyped by sequening on ABI PRISM 3100 instruments, and polymerase chain reaction (PCR) was performed using the GeneAmp PCR system 9700 (Applied Biosystems). Genotype distributions showed no deviation from Hardy–Weinberg equilibrium in cases or controls and, overall, there were no significant differences in allele and genotype frequencies between the schizophrenic patients and controls at any genetic polymorphism. there were still no significant differences in haplotype distribution between cases and controls (globalχ~2= 1.318, P=0.725,d.f.= 3).