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Despite 30–40 years of intense research on a series of promising markers, none has thus far been validated as diagnostic tools or predictors of treatment response. In addition, most of the past approaches were hypothesis driven, relying on our limited knowledge of the pathophysiology of psychiatric disorders. With the sequence of the human genome having being publicly available since February 2001 (Lander et al. 2001; Venter et al. 2001), an array of novel research tools has become available that may yield unbiased, hypothesis-free insight into the pathophysiological underpinnings of certain psychiatric disorders. These novel tools combine knowledge of the sequence of the human genome with miniaturized assays amenable to high-throughput processing for a parallel analysis of the whole genome. Using these, one can investigate the whole genome at the level of the DNA (genomics), all expressed mRNA (expressomics—or, more commonly, expression array or microarray analysis), and all proteins (proteomics) in a single experiment. These three approaches have to deal with increasing levels of complexity, because the approximately 25,000 predicted human genes are expected to give rise to at least 10 times as many protein isoforms with a multitude of posttranslational modifications, such as phosphorylation and glycosylation. Using these unbiased whole genome–based approaches, novel pathways and molecules involved in the pathogenesis of psychiatric disorders may be identified. This chapter will mostly focus on genomewide SNP association studies and their impact on psychiatric genetics; we recommend several reviews on the impact of microarray analysis and proteomics on pathophysiological concepts in psychiatry (Freeman and Hemby 2004; Ginsberg et al. 2004; Mirnics et al. 2006; Tannu and Hemby 2006) for additional information in these areas.

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