Several recent genome-wide network studies in ASD and SCZ do indeed suggest that the disorder risk converges on shared molecular pathways, where currently identified genetic variation is enriched (46). In ASD, these pathways involve the regulation of transcription and chromatin structure during neurogenesis, and subsequent processes of synaptic development and function during early fetal cortical development. Alternative approaches based on protein interactions alone, and the integration of protein, gene expression, or phenotype data, identify similar pathways or show the convergence of multiple ASD risk loci on similar biological processes or networks. A network study of genetic variation underlying SCZ implicates similar risk stages during the development of the prefrontal cortex (63), which is consistent with neuroanatomical and physiological studies.
