The past decade has seen immense progress in psychiatric genetics, with genome-wide association studies (GWAS) having now identified 245 distinct risk loci for SCZ and the demonstration of polygenic influences on SCZ3,4. Polygenic risk scores (PRS) aggregate genetic information from large GWAS3, and index individuals’ polygenic liability for a given trait or disorder in an independent sample. Recent studies have shown that polygenic risk for SCZ influences aspects of executive functioning in individuals with23 and without SCZ24, albeit with limited effect sizes. By harnessing the polygenicity underlying SCZ and genetically correlated disorders (e.g., Bipolar Disorder (BiP) and Major Depressive Disorder (MDD)25), PRS can be leveraged to enhance our understanding of how genetic vulnerability to SCZ may manifest as individual differences in brain activity, providing critical interpretative context for emergent GWAS findings. Large GWAS have demonstrated, using PRS and genome-wide correlations, that there are considerable pleiotropic effects underlying SCZ, bipolar disorder (BiP), and major depressive disorder (MDD)25. By contrasting the SCZ PRS with PRS for genetically correlated disorders, such as BiP and MDD, the specificity and commonality of these genetic vulnerabilities
