Model of common structural genes and their possible contribution to the development of schizophrenia (as thoroughly defined in the Sekar et al. article) Although other diseases (i.e. systemic lupus erythematosus) have been implicated, the<unk>  gene is also being investigated for the role it may play in schizophrenia risk and development. In the Wu et al. study, they utilized the real-time polymerase chain reaction (rt-PCR) as an assay to determine the copy number variance (CNV) or genetic diversity of<unk> . Accordingly, with these results, future prognoses, flares, and remissions will become more feasible to determine. The results basically show copy number variants as a mechanism to effect genetic diversity. As discussed before, the different phenotypes allowed for by the varying genetic variety of complement<unk>  include a wide range of plasma or serum<unk>  proteins among two isotypes—C4A and<unk> B—with multiple protein allotypes that can have unique physiological functions. CNVs are sources of inherent genetic diversity and are engaged in gene-environment interaction. CNVs (and associated polymorphisms) play a role in filling in the gap towards understanding the genetic basis of quantitative traits and the different susceptibilities to autoimmune and neurobiological diseases. Substantial data from all over the world has been collected and analyzed to determine that schizophrenia, indeed, has a strong genetic relationship with a region in the MHC locus on chromosome arm 6. Data and information collected internationally can shed light onto the mysteries of schizophrenia. Sekar et al. analyzed single nucleotide polymorphisms (SNP) of<unk> 0 cohorts in 22 countries, in total adding up to nearly 29,000 cases. They found out two features: 1) A great number of SNPs reaching only 2Mb across the end, 2) peak of association centered at<unk> , predicting that<unk> A expression levels is most strongly correlated with schizophrenia. In addition, they have discovered a mechanism by which schizophrenia could arise from the genetic predisposition of the human complement<unk> . As shown in Figure 1, four common structural variations discovered in genome-wide association studies (GWAS) studies have pointed to the high turnout of schizophrenia. Possibly, the higher levels of expression of<unk>  protein due to pattern of variants of the<unk>  gene, allows for the unwanted increase in synaptic pruning (an effect produced by the effector proteins of the complement system in which the<unk>  partakes).
Complement component 4
Complement component 3
Complement component 5a
Complement receptor 1
Major basic protein
Neutrophil elastase
Macrophage-activating factor
Immunophilins