Schizophrenia is a widespread mental disease that affects about 1% of the world population. Because of the complex heritability of the disease as well as limited knowledge of the precise interconnected biochemical and genetic mechanisms underlying schizophrenia, there is wide variability in terms of antipsychotic drug efficacy, treatment effects, presence and severity of side-effects.
With the completion of the mapping of the human genome, genome-wide association studies (GWAS) bring researchers one step closer to uncovering the molecular associations and pathways involving schizophrenia. Three such current GWAS are examined, as the first GWAS determine genetic associations of 4 candidate genes, the second GWAS explores biological pathways involving histone methylation, immune-neuronal signaling, and the third GWAS attempts to discern the genotypic and phenotypic architecture of schizophrenia.
Other current investigations involve the variability of the SV2C gene, and neurodevelopmental genes DISC1, NRG1, BDNF and NOTCH4. Variability of serotonin and dopamine pathways are also looked at as well as the variability of the CYP enzyme and association of voltage-gated calcium channels with schizophrenia.
Finally current studies dealing with the pharmacogenetic association of genes and antipsychotic side-effects of hyperprolactinemia, extrapyramidal symptoms, QTc prolongation, extreme weight gain, and agranulocytosis are investigated.