Taken together, our results are suggestive of a polygenic association for specific symptom and cognitive dimensions in chronic schizophrenia. This study has several limitations; the obvious one is the sample size which is small in comparison to the recommended n of 2000 (Wray et al., 2014). General limitations of the PRS analysis apply to our study-PRS identifies a polygenic signal but cannot provide specific associations that can help elucidate functional mechanisms. PRS is computed from common variants with small effects, so the contributions of rare and structural variants are not known. Additionally, in our study we only used autosomes for PRS calculations, so effects of common variants in sex chromosomes contributing to polygenic burden are not known. For our set based analysis, we utilized a top SNP approach for the loci analyzed which is a limitation as this could potentially exclude several SNPs that could be causal. Some of these loci are known to have several genes (Ripke et al., 2014).
