The eQTL giving rise to the identified pleiotropic associations between gene expression in the fetal brain and risk for neuropsychiatric disorders do not, for the most part, appear to be fetal-specific. However, their activity within the brain at this timepoint makes it plausible that their pathogenic effects start prenatally, even if they continue into adulthood. Indeed, several of the genes that we implicate are known to have important roles in early brain development. For example, leucine-rich repeat containing genes (which include LRRC37A, implicated in neuroticism, and LRRC57, implicated in bipolar disorder) are known to be key organizers of excitatory and inhibitory synapse formation [53]. Similarly, FLOT1, which exhibited reduced expression in association with genetic risk for schizophrenia, has been found to promote the formation of hippocampal glutamatergic synapses [54], which appear to be decreased in the disorder [55]. Increased expression of C4A in association with schizophrenia risk variation was originally reported in the adult brain [48], where the authors provided data to support a role for this gene in synaptic pruning. Although this process is important for maturation of regions
