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Objective COVID-19 forced third-level students to transition to online learning (OL). Many students encountered issues with OL, such as accessibility. However, the relationship between OL issues and mental health during this time remains poorly understood. Participants: Third-level students in Ireland (N = 268) completed an online questionnaire examining experiences with OL and mental health during COVID-19. Methods: OL social, lecturer, accessibility, individual skills, and environment issues, were entered into logistic regression analyses to examine whether these variables predicted mental health outcomes and/or preference to keep OL. Results: Students reporting more individual skills issues were more likely to attain a probable diagnosis of posttraumatic stress disorder, complex posttraumatic stress disorder, and depression (p < 0.0083); students who reported more environment issues were less likely to report preference to keep OL (p < 0.0005). Conclusions: Given individual skills issues associated with worse mental health, future research should examine improving student perceptions of their own OL skills. [ABSTRACT FROM AUTHOR]

Objective: Mitochondrial dysfunction has been implicated in the pathophysiology of schizophrenia and other neuropsychiatric disorders. Though the exact mechanisms and clinical implications for this dysfunction are not fully determined, there is a hypothesis that deficiency in coenzyme Q10 (CoQ10) may contribute to mitochondrial impairments and be reflected in cognitive, affective, and energy disturbances in the disorders. CoQ10 is a critical component of the mitochondrial respiratory chain and an essential free radical scavenger, necessary for mitochondrial function. Here, we review the results of CoQ10 supplementation interventions for adults with various neurological and neuropsychiatric disorders and consider the therapeutic potential of CoQ10 supplementation for schizophrenia in light of these studies. Methods: A literature review of randomised controlled trials and open-label studies investigating the effect of CoQ10 as a single intervention in adults with neurological and neuropsychiatric disorders was conducted. Results: CoQ10 supplementation has some positive effects on fatigue, cognitive impairment and affective difficulties in several neurological and neuropsychiatric conditions with associated mitochondrial dysfunction. Discussion: CoQ10 may be of therapeutic value to schizophrenia given evidence of mitochondrial dysfunction in the disorder. [ABSTRACT FROM AUTHOR]

Abstract: Working memory‐based cognitive remediation therapy (CT) for psychosis has recently been associated with broad improvements in performance on untrained tasks measuring working memory, episodic memory and IQ, and changes in associated brain regions. However, it is unclear whether these improvements transfer to the domain of social cognition and neural activity related to performance on social cognitive tasks. We examined performance on the Reading the Mind in the Eyes test (Eyes test) in a large sample of participants with psychosis who underwent working memory‐based CT (N = 43) compared to a control group of participants with psychosis (N = 35). In a subset of this sample, we used functional magnetic resonance imaging (fMRI) to examine changes in neural activity during a facial emotion recognition task in participants who underwent CT (N = 15) compared to a control group (N = 15). No significant effects of CT were observed on Eyes test performance or on neural activity during facial emotion recognition, either at p < 0.05 family‐wise error or at a p < 0.001 uncorrected threshold, within a priori social cognitive regions of interest. This study suggests that working memory‐based CT does not significantly impact an aspect of social cognition which was measured behaviourally and neurally. It provides further evidence that deficits in the ability to decode mental state from facial expressions are dissociable from working memory deficits, and suggests that future CT programmes should target social cognition in addition to working memory for the purposes of further enhancing social function. [ABSTRACT FROM AUTHOR]

IMPORTANCE: We investigated the variation in neuropsychological function explained by risk alleles at the psychosis susceptibility gene ZNF804A and its interacting partners using single nucleotide polymorphisms (SNPs), polygenic scores, and epistatic analyses. Of particular importance was the relative contribution of the polygenic score vs epistasis in variation explained. OBJECTIVES: To (1) assess the association between SNPs in ZNF804A and the ZNF804A polygenic score with measures of cognition in cases with psychosis and (2) assess whether epistasis within the ZNF804A pathway could explain additional variation above and beyond that explained by the polygenic score. DESIGN, SETTING, AND PARTICIPANTS: Patients with psychosis (n = 424) were assessed in areas of cognitive ability impaired in schizophrenia including IQ, memory, attention, and social cognition. We used the Psychiatric GWAS Consortium 1 schizophrenia genome-wide association study to calculate a polygenic score based on identified risk variants within this genetic pathway. Cognitive measures significantly associated with the polygenic score were tested for an epistatic component using a training set (n = 170), which was used to develop linear regression models containing the polygenic score and 2-SNP interactions. The best-fitting models were tested for replication in 2 independent test sets of cases: (1) 170 individuals with schizophrenia or schizoaffective disorder and (2) 84 patients with broad psychosis (including bipolar disorder, major depressive disorder, and other psychosis). MAIN OUTCOMES AND MEASURES: Participants completed a neuropsychological assessment battery designed to target the cognitive deficits of schizophrenia including general cognitive function, episodic memory, working memory, attentional control, and social cognition. RESULTS: Higher polygenic scores were associated with poorer performance among patients on IQ, memory, and social cognition, explaining 1% to 3% of variation on these scores (range, P = .01 to .03). Using a narrow psychosis training set and independent test sets of narrow phenotype psychosis (schizophrenia and schizoaffective disorder), broad psychosis, and control participants (n = 89), the addition of 2 interaction terms containing 2 SNPs each increased the R² for spatial working memory strategy in the independent psychosis test sets from 1.2% using the polygenic score only to 4.8% (P = .11 and .001, respectively) but did not explain additional variation in control participants. CONCLUSIONS AND RELEVANCE: These data support a role for the ZNF804A pathway in IQ, memory, and social cognition in cases. Furthermore, we showed that epistasis increases the variation explained above the contribution of the polygenic score. [ABSTRACT FROM AUTHOR]

Background: A single nucleotide polymorphism (rs7914558) within the cyclin M2 (CNNM2) gene was recently identified as a common risk variant for schizophrenia. The mechanism by which CNNM2 confers risk is unknown.Aims: To determine the impact of the rs7914558 risk 'G' allele [corrected] on measures of neurocognition, social cognition and brain structure.Method: Patients with schizophrenia (n = 400) and healthy controls (n = 160) completed measures of neuropsychological function and social cognition. Structural magnetic resonance imaging data were also acquired from an overlapping sample of Irish healthy controls (n = 159) and an independent sample of Italian patients (n = 82) and healthy controls (n = 39).Results: No effects of genotype on neuropsychological test performance were observed. However, a dosage effect of the risk allele was found for an index of social cognition (i.e. attributional style), such that risk status was associated with reduced self-serving bias across groups (GG>AG>AA, P<0.05). Using voxel-based morphometry to investigate neuroanatomical regions putatively supporting social cognition, risk carriers had relatively increased grey matter volume in the right temporal pole and right anterior cingulate cortex (Pcorrected<0.05) in the Irish healthy controls sample; neuroanatomical associations between CNNM2 and grey matter volume in anterior cingulate cortex were also observed in the Italian schizophrenia and healthy controls samples.Conclusions: Although the biological role of CNNM2 in schizophrenia remains unknown, these data suggest that this CNNM2 risk variant rs7914558 may have an impact on neural systems relevant to social cognition. How such effects may mediate the relationship between genotype and disease risk remains to be established. [ABSTRACT FROM AUTHOR]

Objective: The authors investigated the effects of recently identified genome-wide significant schizophrenia genetic risk var- iants on cognition and brain structure. Method: A panel of six single-nucleotide polymorphisms (SNPs) was selected to represent genome-wide significant loci from three recent genome-wide associa- tion studies (GWAS) for schizophrenia and was tested for association with cognitive measures in 346 patients with schizophrenia and 2,342 healthy comparison subjects. Nominally significant results were evaluated for replication in an independent case-control sample. For SNP5 showing evidence of association with cognition, associations with brain structural volumes were investigated in a large independent healthy comparison sample. Results: Five of the six SNPs showed no significant association with any cognitive measure. One marker in the major histocompatibility complex (MHC) region, rs6904071, showed independent, replicated evidence of association with delayed episodic memory and was significant when both samples were combined. In the combined sample of up to 3,100 individuals, this SNP was associated with widespread effects across cognitive domains, although these additional associations were no longer significant after adjusting for delayed episodic memory. In the large independent structural imaging sample, the same SNP was also associated with decreased hippocampal volume. Conclusions: The authors identified a SNP in the MHC region that was associated with cognitive performance in patients with schizophrenia. and healthy comparison subjects. This SNP, rs6904071, showed a replicated association with episodic memory and hippocampal volume. These findings implicate the MHC region in hippocampal structure and functioning, consistent with the role of MHC proteins in synaptic development and function. Follow-up of these results has the potential to provide insights into the pathophysiology of schizophrenia and cognition. [ABSTRACT FROM AUTHOR]

Donohoe G, Duignan A, Hargreaves A, Morris DW, Rose E, Robertson D, Cummings E, Moore S, Gill M, Corvin A. Social cognition in bipolar disorder versus schizophrenia: comparability in mental state decoding deficits. Bipolar Disord 2012: 14: 743-748. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. Objectives: Neuropsychological studies comparing patients with bipolar disorder (BD) to patients with schizophrenia (SZ) suggest milder cognitive deficits in BD patients and across a smaller range of functions. The present study investigated whether this pattern is also true for social cognition - a range of socially relevant abilities, including emotion perception and recognition, theory of mind, and social attributions - by comparing performance on measures of social cognition in patients with BD, SZ, and healthy participants. Methods: One hundred and two patients with BD, 208 patients with SZ, and 132 healthy participants were assessed using a battery of tasks measuring basic neuropsychological and social cognition. Results: We observed significant differences between patients with BD and healthy participants in a test of mental state decoding ('eyes task') that was at a level comparable to deficits seen in patients with SZ. By comparison, BD patients showed more subtle deficits in mental state reasoning ('hinting task') than those shown by patients with SZ. Conclusions: Mental state decoding difficulties are significant in BD. An important direction for further research will be to establish to what extent these deficits affect social and occupational functioning as a potential target for therapeutic intervention. [ABSTRACT FROM AUTHOR]

Background: Coenzyme Q10 (CoQ10) is an endogenous compound that is essential for energy production within the mitochondria and also functions as a potent anti-oxidant, inhibiting oxidative stress and damage. Often deficits in CoQ10 are associated with fatigue, and cognitive and psychological impairment. In light of its many functions, CoQ10 supplementation to minimise decline and improve symptoms has been investigated in multiple disorders including neurological and neuropsychiatric disorders, with results indicating positive effects on fatigue, cognitive impairment and affective difficulties for disorders such as bipolar disorder and chronic fatigue syndrome. There is also evidence of mitochondrial dysfunction in schizophrenia. In light of this evidence, the current study aimed to investigate the potential effect of CoQ10 supplementation on 1) cognitive function and 2) psychological and physical health in schizophrenia and schizoaffective disorder. Methods: A double blind, randomised, placebo controlled study was conducted to assess the effects of CoQ10 supplementation (300mg/day) on cognitive, psychological and physical variables in 70 patients with schizophrenia and schizoaffective disorder. The effects of CoQ10 supplementation were compared to placebo at 3 and 6 months. Plasma CoQ10 was measured at all time points, along with measures of mitochondrial function (via plasma lactate concentration). Sensitivity analysis followed an intention to treat approach that used multiple imputations to account for missing values. Results: Overall there was no effect of CoQ10 supplementation on cognitive outcome measures. This is despite observing an increase in plasma CoQ10 concentration in the CoQ10 group compared to the placebo. CoQ10 supplementation also had no effect on mitochondrial function, energy, psychological symptoms, quality of life, functional status, physical activity or blood pressure at either time point. Discussion: There is considerable evidence that mitochondrial dysfunction is present in patients with schizophrenia and schizoaffective disorder, and this dysfunction is implicated in the manifestation of cognitive impairment and clinical symptoms. CoQ10 can be taken as a nutritional supplement with minimal side effects to target mitochondrial dysfunction via promoting ATP generation and increasing antioxidant capacity. However, we found no effect of CoQ10 supplementation on any variable under investigation. It is possible that CoQ10 might act as a protective agent against exacerbated oxidative stress in these patients, and future studies might be warranted to examine this possibility. However, the current data is conclusive that CoQ10 supplementation does not ameliorate existing deficits in schizophrenia. These findings are translatable to clinical and community settings. [ABSTRACT FROM AUTHOR]