June 4, 2015

Novel Findings from CNVs Implicate Inhibitory and Excitatory Signaling Complexes in Schizophrenia




Introduction

(June 4, 2015)   Schizophrenia is a highly heritable disorder, the genetic architecture of which includes a large number of alleles spanning the full spectrum of frequencies. It has been estimated that the additive effects of common variation, as indexed by alleles represented on the platforms used in genome-wide association studies (GWASs), contribute around a quarter to a third of the total population variance in schizophrenia liability. However, the 108 genome-wide-associated common variant loci reported in the largest GWAS study to date only explain a small fraction of this contribution. An increased burden of rare mutations has also been documented in schizophrenia, taking the form of both large CNVs and single-nucleotide variants (SNVs), which often occur as de novo mutations. While several CNVs have been implicated in the disorder, no individual SNV has yet been robustly associated. The CNVs (n = 11) strongly associated with schizophrenia in the largest systematic survey to date are in general large in both size (> 500 kb) and effect (ORs 2–60), the latter being in stark contrast with the small effects conferred by common alleles (typical OR < 1.1).

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