Quantitative SZ-BD cognitive differences commonly seen using group averages did not hold when cognitive heterogeneity was factored into our sample. Members of each corresponding subgroup, irrespective of diagnosis, might be manifesting the outcome of differences in shared cognitive risk factors.

Individuals with schizophrenia display substantial deficits in social functioning (SF), characterized by chronic, lifelong presentations. Yet, at present there are few effective interventions to enhance SF in this population. Emerging evidence from studies of clinical populations that display similar SF deficits suggests that aerobic exercise (AE) may improve social skills. However, this putative impact has not been investigated in schizophrenia. Employing a single-blind, randomized clinical trial design, 33 individuals with schizophrenia were randomized to receive 12 weeks of Treatment-As-Usual (TAU; n = 17) or TAU + AE (n = 16) utilizing active-play video games (Xbox 360 Kinect) and traditional AE equipment. Participants completed an evaluation of aerobic fitness (VO 2 max) as well as self-, informant-, and clinician-reported SF measures at baseline and after 12 weeks. Twenty-six participants completed the study (79%; TAU = 13; AE = 13). At follow-up, the AE participants improved their VO 2 max by 18.0% versus − 0.5% in the controls (group x time interaction, F 1,24 = 12.88; p = .002). Hierarchical stepwise regression analyses indicated improvements in VO 2 max significantly predicted enhancement in SF as indexed by self-, informant-, and clinician-reported measures, predicting 47%, 33%, and 25% of the variance, respectively (controlling for baseline demographics, medications, mood symptoms, and social networks). Compared to the TAU group, AE participants reported significant improvement in SF (23.0% vs. − 4.2%; group × time interaction, F 1,24 = 7.48, p = .012). The results indicate that VO 2 max enhancement leads to improvements in SF in people with schizophrenia. Furthermore, low VO 2 max represents a modifiable risk factor of SF in people with schizophrenia, for which AE training offers a safe, non-stigmatizing, and nearly side-effect-free intervention.

Decreased expression of oligodendrocyte/myelin-related (OMR) genes, including quaking (QKI), is a consistent finding in gene expression studies of post-mortem brain from subjects with schizophrenia, and these changes are most prominent in the hippocampus vs. the prefrontal cortex (PFC). Although expression of QKI and other OMR genes has been examined in rodents, little is known about their developmental trajectory in the human brain. Therefore, we examined expression of QKI and several putative mRNA targets of QKI in human PFC and hippocampus at different ages. The pattern of QKI expression in the PFC resembled that reported in rodents, with high QKI-5 in the fetal brain and an increase in QKI-6 and QKI-7 during the period of active myelination, although QKI-5 expression did not decrease substantially during postnatal development in the PFC in humans as it does in rodent brain. Most of the putative QKI target genes also showed linear increases in expression with increasing age in the PFC. In contrast, expression of these genes showed little evidence of developmental regulation in the hippocampus. Correlations between expression levels of the nuclear vs. cytoplasmic QKI isoforms, and putative splicing targets of the former, also differed between tissues. Thus, we speculate that a robust increase in OMR gene expression normally occurs with age in the PFC, but not in the hippocampus, which may explain why decreases in OMR gene expression in schizophrenia are more pronounced in the latter tissue. We also suggest that OMR transcripts might be processed by different splicing proteins in different tissues.

Emotion regulation (ER) difficulties are ubiquitous among individuals with schizophrenia and have been hypothesized to contribute to stress sensitivity and exacerbation of psychotic symptoms in this population. However, the evidence supporting this link is equivocal, potentially due to previous studies' reliance on retrospective assessments of ER and psychosis, as well as lack of consideration of putative moderators such as emotion awareness. To address these limitations, we employed experience sampling method using mobile electronic devices to investigate the links between momentary in vivo use of ER strategies (m ER), emotion awareness, and psychotic symptoms during daily functioning. Fifty-four individuals with schizophrenia completed assessment of m ER and psychotic symptoms, along with traditional retrospective measures of ER and symptoms. Use of m ER suppression predicted significant increases in momentary experiences of thought insertion, mind reading, auditory and visual hallucinations. Use of m ER reappraisal predicted significant increases in momentary experiences of suspiciousness, thought insertion, and mind reading. Emotion awareness, driven primarily by difficulties identifying feelings, moderated the impact of ER on psychotic symptoms. There were no associations between retrospective measures of ER and symptoms. Our results indicate that, among individuals with schizophrenia, emotion awareness significantly impacts the relationship between use of ER and exacerbations in psychotic symptoms during the course of daily functioning. Our results highlight the need to incorporate emotion awareness and regulation difficulties into the development of treatment models and interventions for psychosis. In addition, our results underscore the need to employ in vivo, high time-resolution assessment methods to study dynamic clinical phenomena such as ER and psychotic symptoms.

The relationship between neurocognition and community functioning in BD may be dependent on social cognition status, implying the presence of social cognitive heterogeneity. Results may be relevant to choosing proper treatment interventions depending on the patient's social cognitive level.