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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]

ImportanceWe 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.ObjectivesTo (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 participantsPatients 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 measuresParticipants 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.ResultsHigher 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 relevanceThese 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.

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]

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]