Suicide is a major public health problem, and it is urgent to investigate its underlying clinical and psychological concomitants. It has been suggested that low mentalization skills and problematic use of the internet (PUI) are factors that can play a role in suicidal behaviors. It is possible that poor mentalization skills contribute to leading to forms of PUI, which, in turn, can represent triggers for suicidal ideation (SI). We tested this hypothesis through a quantitative and cross-sectional study on a sample (n = 623) of young adults (age range: 18–34). Self-report measures investigating symptoms related to Social Media Addiction (SMA), Internet Gaming Disorder (IGD), mentalization capacity, and SI were used. A single mediation analysis with two mediators was carried out to evaluate the direct and indirect effects of mentalization on SI through the mediating role of SMA- and IGD-related symptoms, controlling for potential confounding factors (e.g., socio-demographic and addiction-related variables). The four explored variables were significantly associated with each other (all p < 0.001) across all subjects; the mediational model showed that the total effect of mentalization on SI was significant (B = −0.821, SE = 0.092 (95% CI: −1.001; −0.641)) and that both SMA- (B = −0.073, SE = 0.034 (95% CI: −0.145; −0.008)) and IGD-related symptoms (B = 0.046, SE = 0.027 (95% CI: −0.107; −0.001)) were significant mediators of such association. Our findings support the possibility that PUI severity plays a relevant role in mediating the association between low mentalization skills and levels of SI.

Background. Insufficient effectiveness and a difficult tolerability profile of antidepressant drugs for the treatment of major depressive disorder (MDD) have been reported, and polyunsaturated fatty acids (PUFAs) have been posited as reliable therapeutic alternatives. The present study investigated the efficacy of omega‐3 PUFAs as monotherapy for MDD. Methods. Two well‐trained reviewers independently looked at the most significant randomized clinical trials (RCTs) from the PubMed database regarding PUFAs’ employment in MDD compared to placebo; “major depressive disorder” and “omega‐3 fatty acids,” or “omega‐6 fatty acids,” or “polyunsaturated fatty acids (PUFA),” or “n − 3 polyunsaturated fatty acids,” or “eicosapentaenoic acid (EPA),” or “docosahexaenoic acid (DHA)” were used as the medical subject keywords. Results. Of the initial 96 potential RCTs based on titles and abstracts, 82 studies did not meet the inclusion criteria and were excluded. Six studies were excluded from the remaining 14 after full text revision. Eight RCTs met all the inclusion/exclusion criteria without reporting clear evidence of PUFAs’ effectiveness in the treatment of MDD. Conclusion. At present, there is no opportunity to recommend the use of omega‐3 PUFAs monotherapy for the treatment of MDD, although their supplementation may be useful in some specific populations.

Patients with the 22q11.2 deletion syndrome (DS) show an increased risk of developing a psychotic illness lifetime. 22q11.2DS may represent a reliable model for studying the neurobiological underpinnings of schizophrenia. The study of social inference abilities in a genetic condition at high risk for psychosis, like 22q11.2DS, may shed light on the relationships between neurocognitive processes and patients' daily general functioning. The study sample consisted of 1736 participants, divided into four groups: 22q11.2DS patients with diagnosis of psychotic disorder (DEL SCZ, N = 20); 22q11.2DS subjects with no diagnosis of psychosis (DEL, N = 43); patients diagnosed with schizophrenia without 22q11.2DS (SCZ, N = 893); and healthy controls (HC, N = 780). Social cognition was assessed through The Awareness of Social Inference Test (TASIT) and general functioning through the Specific Levels of Functioning (SLoF) scale. We analysed data through regression analysis. The SCZ and DEL groups had similar levels of global functioning; they both had significantly lower SLoF Total scores than HC ( p < .001); the DEL SCZ group showed significantly lower scores compared to the other groups (SCZ, p = .004; DEL, p = .003; HC, p < .001). A significant deficit in social cognition was observed in the three clinical groups. In the DEL SCZ and SCZ groups, TASIT scores significantly predicted global functioning ( p < .05). Our findings of social cognition deficit in psychosis‐prone patients point to the possible future adoption of rehabilitation programmes, like Social Skills Training and Cognitive Remediation, during premorbid stages of psychosis.

Background: There is a growing body of literature on the association between psychosis and sexual dysfunction. However, most studies have focused on sexual dysfunction and have not investigated the sexual lives of patients with psychosis across a broader range. Material and Methods: Consecutive patients with a diagnosis of acute psychosis or schizophrenia were recruited to the study after obtaining informed consent (n = 46). In addition, healthy control subjects were recruited (n = 52). Sociodemographic and clinical data, psychopathology, and sexual functioning were assessed. Independent sample t-test to determine group differences was obtained. Results: In both the male and female groups, there are significant differences between psychotic individuals and healthy controls in several areas of their sexual functioning: the control group seemed to better perceive Couple sexuality, Self-eroticism, and overall appeared to have a higher Quality of sexual life; on the other hand, the group of patients with psychosis displayed higher scores in Sexual dysfunction. Conclusions: A poor sexual quality of life may be found in patients with psychotic disorders. Assessment of sexual function in these patients is necessary to identify and manage issues and provide support and help to patients in this important area of life.

Background Social cognition (SC) deficits and of its facial emotion expression (FEE) component have been described in 22q11.2 Deletion Syndrome (22q11.2DS), a high-risk for schizophrenia (SCZ) systemic genetic syndrome. Correlations between deficits in FEE skills and visual-spatial abilities in people with 22q11.2DS warrant investigation. Methods The sample consisted of 37 patients with 22q11.2DS (DEL), 19 with 22q11.2DS and psychosis (DEL-SCZ), 23 with idiopathic SCZ, and 48 healthy controls. We assessed FEE through The Ekman 60 Faces test (EK-F60), visual-spatial skills with Raven's Standard Progressive Matrices, and symptom severity with the positive And negative syndrome scale. Statistics were conducted through multivariate analysis of variance and correlation analysis. Results Patients with 22q11.2DS performed worse that the other groups in recognizing Surprise, Disgust, Rage, Fear, and Neutral expressions on the EK-F60. Recognition of Surprise and Disgust correlated positively with visual-spatial abilities in patients with 22q11.2DS; negative and cognitive symptoms correlated negatively with recognition of Sadness, Surprise, and Disgust. Conclusions Patients with 22q11.2DS show impairments of both peripheral and central steps of the emotional recognition process, leading to SC deficits. The latter are present regardless of the presence of a full-blown psychosis.

Background: The phenotypic expression of 22q11.2 deletion syndrome (22q11.2DS) is variable and may include cognitive, psychiatric, and neurological manifestations, e.g., parkinsonism. We investigated brain structural alterations in patients with 22q11.2DS with and without parkinsonism (Park+ and Park−) in comparison with healthy controls (HCs). Methods: Voxel-based morphometry was performed on 3D T1-weighted MR images to explore gray matter volume (GMV) differences between 29 patients (15 Park+, 14 Park−), selected from a consecutive series of 56 adults diagnosed with 22q11.2DS, and 24 HCs. One-way ANOVA and multiple linear regression analyses were performed to explore group differences in GMV and correlations between clinical scores (MDS-UPDR-III and MoCA scores) and structural alterations. Results: Significant between-group differences in GMV were found in the cerebellum, specifically in bilateral lobes VIII and left Crus II, as well as in the left superior occipital gyrus. Although both Park+ and Park− patients showed GMV decrements in these regions with respect to HCs, GMV loss in the right lobe VIII and left Crus II was greater in Park+ than in Park− patients. GMV loss did not correlate with clinical scores. Conclusions: Patients with 22q11.2DS and parkinsonism manifest specific cerebellar volume alterations, supporting the hypothesis of neurodegenerative processes in specific cerebellar regions as a putative pathophysiological mechanism responsible for parkinsonism in patients with 22q11.2DS.