thickness and volume (French et al., 2015, Van der Auwera et al., 2017). Other studies have begun to link SCZ PRS to functional imaging phenotypes such as reward- and working memory-related brain function; however results thus far have been mixed and are often derived from small samples (Lancaster et al., 2016b, Erk et al., 2017, Lancaster et al., 2016a). Overall, this evidence suggests that some neural phenotypes associated with schizophrenia may represent neural mechanisms of common polygenic liability. However, other evidence, drawn from large samples, suggests minimal genomic overlap between subcortical brain volume and schizophrenia (Franke et al., 2016). Lastly, a recent study reports that SCZ-PRS are associated with differentially methylated probes in postmortem tissues from the prefrontal cortex, striatum and cerebellum of schizophrenic and control decedents (Viana et al., 2017). The most significantly associated probe was within DISC1, a gene associated with schizophrenia. Such studies provide exciting new opportunities for linking static genomic variation, in their polygenic form, to epigenetic variation.
