53 research outputs found

    More haste less speed: A meta-analysis of thinking latencies during planning in people with psychosis

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    Cognitive impairment is a core feature of psychosis, with slowed processing speed thought to be a prominent impairment in schizophrenia and first-episode psychosis. However, findings from the Stockings of Cambridge (SOC) planning task suggest changes in processing speed associated with the illness may include faster responses in early stages of planning, though findings are inconsistent. This review uses meta-analytic methods to assess thinking times in psychosis across the available literature. Studies were identified by searching PubMed, Web of Science and Google Scholar. Eligibility criteria: 1) included a sample of people with non-affective psychosis according to DSM III, DSM IV, DSM V or ICD-10 criteria; 2) employed the SOC task; 3) included a healthy control group; and 4) published in English. We identified 11 studies that employed the SOC task. Results show that people with psychosis have significantly faster initial thinking times than non-clinical participants, but significantly slower subsequent thinking times during problem execution. These findings indicate that differences in processing speed are not limited to slower responses in people with psychosis but may reflect a preference for step-by-step processing rather than planning before task execution. We suggest this style of responding is adopted to compensate for working memory impairment

    Interaction Testing and Polygenic Risk Scoring to Estimate the Association of Common Genetic Variants with Treatment Resistance in Schizophrenia

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    Importance: About 20% to 30% of people with schizophrenia have psychotic symptoms that do not respond adequately to first-line antipsychotic treatment. This clinical presentation, chronic and highly disabling, is known as treatment-resistant schizophrenia (TRS). The causes of treatment resistance and their relationships with causes underlying schizophrenia are largely unknown. Adequately powered genetic studies of TRS are scarce because of the difficulty in collecting data from well-characterized TRS cohorts. Objective: To examine the genetic architecture of TRS through the reassessment of genetic data from schizophrenia studies and its validation in carefully ascertained clinical samples. Design, Setting, and Participants: Two case-control genome-wide association studies (GWASs) of schizophrenia were performed in which the case samples were defined as individuals with TRS (n = 10501) and individuals with non-TRS (n = 20325). The differences in effect sizes for allelic associations were then determined between both studies, the reasoning being such differences reflect treatment resistance instead of schizophrenia. Genotype data were retrieved from the CLOZUK and Psychiatric Genomics Consortium (PGC) schizophrenia studies. The output was validated using polygenic risk score (PRS) profiling of 2 independent schizophrenia cohorts with TRS and non-TRS: a prevalence sample with 817 individuals (Cardiff Cognition in Schizophrenia [CardiffCOGS]) and an incidence sample with 563 individuals (Genetics Workstream of the Schizophrenia Treatment Resistance and Therapeutic Advances [STRATA-G]). Main Outcomes and Measures: GWAS of treatment resistance in schizophrenia. The results of the GWAS were compared with complex polygenic traits through a genetic correlation approach and were used for PRS analysis on the independent validation cohorts using the same TRS definition. Results: The study included a total of 85490 participants (48635 [56.9%] male) in its GWAS stage and 1380 participants (859 [62.2%] male) in its PRS validation stage. Treatment resistance in schizophrenia emerged as a polygenic trait with detectable heritability (1% to 4%), and several traits related to intelligence and cognition were found to be genetically correlated with it (genetic correlation, 0.41-0.69). PRS analysis in the CardiffCOGS prevalence sample showed a positive association between TRS and a history of taking clozapine (r2 = 2.03%; P =.001), which was replicated in the STRATA-G incidence sample (r2 = 1.09%; P =.04). Conclusions and Relevance: In this GWAS, common genetic variants were differentially associated with TRS, and these associations may have been obscured through the amalgamation of large GWAS samples in previous studies of broadly defined schizophrenia. Findings of this study suggest the validity of meta-analytic approaches for studies on patient outcomes, including treatment resistance

    S-10-2 Are primary negative symptoms treatable?

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    New generation of antidepressants

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    Four behavioural syndromes of schizophrenia

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