Search

Background Social cognition may be critical to the impoverished social functioning seen in serious mental illness. However, although social-cognitive deficits are consistently demonstrated in schizophrenia spectrum disorders (SSD), studies in bipolar disorder (BD) have produced inconsistent results. This inconsistency may relate to symptom profiles of patients studied, particularly the presence or absence of psychotic features. Thus, we examined social cognition in bipolar disorder with psychotic features (BD +) versus without psychotic features (BD −) relative to SSD and controls. Methods A sample of 537 SSD patients, 85 BD + patients, 37 BD − patients, and 309 controls were administered the MATRICS Consensus Cognitive Battery, including a social cognition measure, the managing emotions branch of the Mayer–Salovey–Caruso Emotional Intelligence Test (MSCEIT). Analyses of covariance compared MSCEIT performance between diagnostic groups while controlling for race, psychotropic medication status, and neurocognition. Results SSD but not BD − or BD + patients showed significant MSCEIT deficits relative to controls. Conclusions MSCEIT deficits were found in SSD but not BD − or BD +, suggesting that social cognition may represent an underlying difference between SSD and BD. However, variance in MSCEIT performance among BD patients may also suggest latent BD subgroups characterized by social-cognitive deficits. Findings can help inform future investigations into how social cognition and social brain development differ between SSD and BD.

It has long been recognized that generalized deficits in cognitive ability represent a core component of schizophrenia, evident prior to full illness onset and independent of medication. The possibility of genetic overlap between risk for schizophrenia and cognitive phenotypes has been suggested by the presence of cognitive deficits in first-degree relatives of patients with schizophrenia; however, until recently, molecular genetic approaches to test this overlap have been lacking. Within the last few years, large-scale genome-wide association studies (GWAS) of schizophrenia have demonstrated that a substantial proportion of the heritability of the disorder is explained by a polygenic component consisting of many common SNPs of extremely small effect. Similar results have been reported in GWAS of general cognitive ability. The primary aim of the present study is to provide the first molecular genetic test of the classic endophenotype hypothesis, which states that alleles associated with reduced cognitive ability should also serve to increase risk for schizophrenia. We tested the endophenotype hypothesis by applying polygenic SNP scores derived from a large-scale cognitive GWAS meta-analysis (~5000 individuals from 9 non-clinical cohorts comprising the COGENT consortium) to four schizophrenia case-control cohorts. As predicted, cases had significantly lower cognitive polygenic scores compared to controls. In parallel, polygenic risk scores for schizophrenia were associated with lower general cognitive ability. Additionally, using our large cognitive meta-analytic dataset, we identified nominally significant cognitive associations for several SNPs that have previously been robustly associated with schizophrenia susceptibility. Results provide molecular confirmation of the genetic overlap between schizophrenia and general cognitive ability, and may provide additional insight into pathophysiology of the disorder.