Individuals with schizophrenia display substantial neurocognitive deficits for which available treatments offer only limited benefits. Yet, findings from studies of animals, clinical and nonclinical populations have linked neurocognitive improvements to increases in aerobic fitness (AF) via aerobic exercise training (AE). Such improvements have been attributed to up-regulation of brain-derived neurotrophic factor (BDNF). However, the impact of AE on neurocognition, and the putative role of BDNF, have not been investigated in schizophrenia. Employing a proof-of-concept, single-blind, randomized clinical trial design, 33 individuals with schizophrenia were randomized to receive standard psychiatric treatment (n = 17; "treatment as usual"; TAU) or attend a 12-week AE program (n = 16) utilizing active-play video games (Xbox 360 Kinect) and traditional AE equipment. Participants completed assessments of AF (indexed by VO2 peak ml/kg/min), neurocognition (MATRICS Consensus Cognitive Battery), and serum-BDNF before and after and 12-week period. Twenty-six participants (79%) completed the study. At follow-up, the AE participants improved their AF by 18.0% vs a -0.5% decline in the TAU group (P = .002) and improved their neurocognition by 15.1% vs -2.0% decline in the TAU group (P = .031). Hierarchical multiple regression analyses indicated that enhancement in AF and increases in BDNF predicted 25.4% and 14.6% of the neurocognitive improvement variance, respectively. The results indicate AE is effective in enhancing neurocognitive functioning in people with schizophrenia and provide preliminary support for the impact of AE-related BDNF up-regulation on neurocognition in this population. Poor AF represents a modifiable risk factor for neurocognitive dysfunction in schizophrenia for which AE training offer a safe, nonstigmatizing, and side-effect-free intervention.

Successful social functioning requires adaptive forms of emotion awareness and regulation. However, despite well-documented deficits in social functioning in individuals with schizophrenia, little is known about emotion awareness and regulation in this population. Therefore, we compared emotion awareness and regulation in individuals with schizophrenia and healthy controls, and then, within the schizophrenia group, we examined their impact on social functioning. Forty-four individuals with schizophrenia and 20 healthy controls completed measures of emotion awareness, emotion regulation, and social functioning, in addition to control measures, including neurocognitive functioning. Compared to controls, individuals with schizophrenia displayed significant deficits describing and identifying their emotions and used significantly less reappraisal and more suppression to regulate their emotions. Among the schizophrenia group, better social functioning was associated with the ability to identify, and in particular to describe emotions, better emotion management, as well as greater use of reappraisal and less use of suppression. A hierarchical multiple regression analysis indicated that, after controlling for age and neurocognition, difficulties describing feelings accounted for 35% of the social functioning variance. The present study highlights the importance of emotion awareness and regulation in schizophrenia, pointing to their substantial influence on social functioning above and beyond the impact of neurocognitive functioning.

Background Social dysfunction is a hallmark symptom of schizophrenia which commonly precedes the onset of psychosis. It is unclear if social symptoms in clinical high-risk patients reflect depressive symptoms or are a manifestation of negative symptoms. Method We compared social function scores on the Social Adjustment Scale-Self Report between 56 young people (aged 13–27 years) at clinical high risk for psychosis and 22 healthy controls. The cases were also assessed for depressive and ‘prodromal’ symptoms (subthreshold positive, negative, disorganized and general symptoms). Results Poor social function was related to both depressive and negative symptoms, as well as to disorganized and general symptoms. The symptoms were highly intercorrelated but linear regression analysis demonstrated that poor social function was primarily explained by negative symptoms within this cohort, particularly in ethnic minority patients. Conclusions Although this study demonstrated a relationship between social dysfunction and depressive symptoms in clinical high-risk cases, this association was primarily explained by the relationship of each of these to negative symptoms. In individuals at heightened risk for psychosis, affective changes may be related to a progressive decrease in social interaction and loss of reinforcement of social behaviors. These findings have relevance for potential treatment strategies for social dysfunction in schizophrenia and its risk states and predict that antidepressant drugs, cognitive behavioral therapy and/or social skills training may be effective.