Genome wide association study on memory in schizophrenia patients and unaffected healthy volunteers

The knowledge resulting from the complete sequence of the human genome, the identification of single nucleotide polymorphisms (SNPs), and the development of parallel genotyping technology (microarrays) established the conditions that brought about the current revolution in our ability to probe the genome for identifying disease genes. Genome-wide association (GWA) studies have opened a window into the biology of common complex diseases and yielded several genes showing strong association with complex diseases including Crohn's disease, diabetes and many others. These studies revealed genes involved in pathogenesis and identified unexpected disease pathways. This knowledge could translate into the development of better treatment or even cure. There is evidence for a strong genetic component in the etiology of schizophrenia, as demonstrated by family, twin and adoption studies. The risk of developing the disease increases with the genetic relatedness to an individual suffering from the disorder. Furthermore, schizophrenic patients, their unaffected relatives display alterations in various intermediate phenotypes. We use complementary strategies to approach the pathobiology and genetics of schizophrenia including genetic association studies on schizophrenia and schizophrenia-related intermediate phenotypes as well as animal and cell culture models. The poster will present a genome-wide association study including 550 patients and 550 controls concentrating on memory parameters.