Mentalizing—our ability to make inferences about the mental states of others—is impaired across psychiatric disorders and robustly associated with functional outcomes. Mentalizing deficits have been prominently linked to aberrant activity in cortical regions considered to be part of the “social brain network” (e.g., dorsomedial prefrontal cortex, temporoparietal junction), yet emerging evidence also suggests the importance of cerebellar dysfunction. In the present study—using a transdiagnostic, clinical psychiatric sample spanning the psychosis-autism-social anxiety spectrums—we examined the role of the cerebellum in mentalizing and its unique contributions to broader social functioning.

Sixty-two participants (38 with significant social dysfunction secondary to psychiatric illness and 24 nonclinical controls without social dysfunction) completed a mentalizing task during functional magnetic resonance imaging. General linear model analysis, latent variable modeling, and regression analyses were used to examine the contribution of cerebellum activation to the prediction of group status and social functioning.

Mentalizing activated a broad set of social cognitive brain regions, including cerebral mentalizing network (MN) nodes and posterior cerebellum. Higher posterior cerebellum activation significantly predicted clinical status (i.e., individuals with psychiatric disorders versus nonclinical controls). Finally, cerebellar activation accounted for significant variance in social functioning independent of all other cerebral MN brain regions identified in a whole-brain analysis.

Findings add to an accumulating body of evidence establishing the unique role of the posterior cerebellum in mentalizing deficits and social dysfunction across psychiatric illnesses. Collectively, our results suggest that the posterior cerebellum should be considered – alongside established cerebral regions – as part of the mentalizing network.

Differences in social behaviours are common in young people with neurodevelopmental conditions (NDCs). Recent research challenges the long-standing hypothesis that difficulties in social cognition explain social behaviour differences.

We examined how difficulties regulating one's behaviour, emotions and thoughts to adapt to environmental demands (i.e. dysregulation), alongside social cognition, explain social behaviours across neurodiverse young people.

We analysed cross-sectional behavioural and cognitive data of 646 6- to 18-year-old typically developing young people and those with NDCs from the Province of Ontario Neurodevelopmental Network. Social behaviours and dysregulation were measured by the caregiver-reported Adaptive Behavior Assessment System Social domain and Child Behavior Checklist Dysregulation Profile, respectively. Social cognition was assessed by the Neuropsychological Assessment Affect-Recognition and Theory-of-Mind, Reading the Mind in the Eyes Test, and Sandbox continuous false-belief task scores. We split the sample into training (n = 324) and test (n = 322) sets. We investigated how social cognition and dysregulation explained social behaviours through principal component regression and hierarchical regression in the training set. We tested social cognition-by-dysregulation interactions, and whether dysregulation mediated the social cognition–social behaviours association. We assessed model fits in the test set.

Two social cognition components adequately explained social behaviours (13.88%). Lower dysregulation further explained better social behaviours (β = −0.163, 95% CI −0.191 to −0.134). Social cognition-by-dysregulation interaction was non-significant (β = −0.001, 95% CI −0.023 to 0.021). Dysregulation partially mediated the social cognition–social behaviours association (total effect: 0.544, 95% CI 0.370–0.695). Findings were replicated in the test set.

Self-regulation, beyond social cognition, substantially explains social behaviours across neurodiverse young people.

Adult patients with the genetic disease neurofibromatosis type 1 (NF1) frequently report social difficulties. To date, however, only two studies have explored whether these difficulties are caused by social cognition deficits, and these yielded contradictory data. The aim of the present study was to exhaustively assess social cognition abilities (emotion, theory of mind, moral reasoning, and social information processing) in adults with NF1, compared with a control group, and to explore links between social cognition and disease characteristics (mode of inheritance, severity, and visibility).

We administered a social cognition battery to 20 adults with NF1 (mean age = 26.5 years, SD = 7.4) and 20 healthy adults matched for sociodemographic variables.

Patients scored significantly lower than controls on emotion, theory of mind, moral reasoning, and social information processing tasks. No effects of disease characteristics were found.

These results appear to confirm that adults with NF1 have a social cognition weaknesses that could explain, at least in part, their social difficulties, although social abilities are not all impaired to the same extent. Regarding the impact of the disease characteristics, the patient sample seemed slightly insufficient for the power analyses performed. Thus, this exploratory study should form the basis of further research, with the objective of replicating these results with larger and more appropriately matched samples.

Older adults are identified to have reduced social cognitive performance compared to younger adults. However, few studies have examined age-associations throughout later life to determine whether these reductions continue with advancing age.

This study assesses cross-sectional associations of emotion perception, cognitive and affective theory of mind (ToM), and emotional empathy in a healthy sample of 157 adults aged 50–89 years (M = 65.31, SD = 9.00, 68% female sex). Emotion perception, cognitive ToM, and affective ToM were measured using The Awareness of Social Inference Test Short Form (TASIT-S), while affective ToM was also measured using Reading the Mind in the Eyes Revised (RME-R). Emotional empathy was measured using the Empathy Quotient.

Multiple regression analyses, adjusting for multiple comparisons, revealed a moderate negative association between age and emotion perception for all emotions combined, as well as for sad and revolted expressions, but not happy, neutral, anxious, or angry expressions. Age had a negative, moderate association with first-order cognitive, second-order cognitive, and affective ToM measured using TASIT-S, but not RME-R. Age was not significantly associated with emotional empathy.

This study contributes to the limited understanding of age-related associations of social cognitive performance throughout later life. This knowledge can inform future research examining the clinical utility of including social cognitive measures in neuropsychological screening and diagnostic tools for later-life neurological disorders.

Altered affective state recognition is assumed to be a root cause of aggressive behavior, a hallmark of psychopathologies such as psychopathy and antisocial personality disorder. However, the two most influential models make markedly different predictions regarding the underlying mechanism. According to the integrated emotion system theory (IES), aggression reflects impaired processing of social distress cues such as fearful faces. In contrast, the hostile attribution bias (HAB) model explains aggression with a bias to interpret ambiguous expressions as angry.

In a set of four experiments, we measured processing of fearful and angry facial expressions (compared to neutral and other expressions) in a sample of 65 male imprisoned violent offenders rated using the Hare Psychopathy Checklist-Revised (PCL-R, Hare, R. D. (1991). The psychopathy checklist–revised. Toronto, ON: Multi-Health Systems) and in 60 age-matched control participants.

There was no evidence for a fear deficit in violent offenders or for an association of psychopathy or aggression with impaired processing of fearful faces. Similarly, there was no evidence for a perceptual bias for angry faces linked to psychopathy or aggression. However, using highly ambiguous stimuli and requiring explicit labeling of emotions, violent offenders showed a categorization bias for anger and this anger bias correlated with self-reported trait aggression (but not with psychopathy).

These results add to a growing literature casting doubt on the notion that fear processing is impaired in aggressive individuals and in psychopathy and provide support for the idea that aggression is related to a hostile attribution bias that emerges from later cognitive, post-perceptual processing stages.

Previous studies have found deficits in imaginative elaboration and social inference to be associated with agenesis of the corpus callosum (ACC; Renteria-Vasquez et al., 2022; Turk et al., 2009). In the current study, Thematic Apperception Test (TAT) responses from a neurotypical control group and a group of individuals with ACC were used to further study the capacity for imaginative elaboration and story coherence.

Topic modeling was employed utilizing Latent Diritchlet Allocation to characterize the narrative responses to the pictures used in the TAT. A measure of the difference between models (perplexity) was used to compare the topics of the responses of individual participants to the common core model derived from the responses of the control group. Story coherence was tested using sentence-to-sentence Latent Semantic Analysis.

Group differences in perplexity were statistically significant overall, and for each card individually (p < .001). There were no differences between the groups in story coherence.

TAT narratives from persons with ACC were normally coherent, but more conventional (i.e., more similar to the core text) compared to those of neurotypical controls. Individuals with ACC can make conventional social inferences about socially ambiguous stimuli, but are restricted in their imaginative elaborations, resulting in less topical variability (lower perplexity values) compared to neurotypical controls.

Although obsessive–compulsive disorder (OCD) is highly prevalent in schizophrenia, its relationship with patients’ real-life functioning is still controversial.

The present study aims at investigating the prevalence of OCD in a large cohort of non-preselected schizophrenia patients living in the community and verifying the relationship of OCD, as well as of other psychopathological symptoms, with real-life functioning along a continuum of OCD severity and after controlling for demographic variables.

A sample of 327 outpatients with schizophrenia was enrolled in the study and collapsed into three subgroups according to OCD severity (subclinical, mild–moderate, severe). A series of structural equation modeling (SEM) was performed to analyze in each subgroup the association of obsessive–compulsive symptoms with real-life functioning, assessed through the Specific Levels of Functioning Scale and the UCSD Performance-Based Skills Assessment. Moreover, latent profile analysis (LPA) was performed to infer latent subpopulations. In the subclinical OCD group, obsessive–compulsive symptoms (OCS) were not associated with functioning, whereas in the mild–moderate OCD group, they showed a positive relationship, particularly in the domains of work and everyday life skills. The paucity of patients with severe OCD did not allow performing SEM analysis in this group. Finally, LPA confirmed a subgroup with mild–moderate OCS and more preserved levels of functioning.

These findings hint at a positive association between mild–moderate OCD and real-life functioning in individuals with schizophrenia and encourage a careful assessment of OCD in personalized programs to sustain daily life activities.