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      Migration Status, Familial Risk for Mental Disorder, and Schizotypal Personality Traits

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          Abstract

          Markedly raised incidence rates of schizophrenia and other psychotic disorders have been observed in several migrant and ethnic minority groups. To contribute to a better understanding of the elevated risk for psychotic disorders that is conferred by migration status, the present study examined effects associated with migration risk status on schizotypal personality traits, which are thought to reflect an underlying vulnerability to psychotic disorder. Effects of migration status were also compared to effects associated with a family history of psychopathology, which represents a robust nonspecific risk factor. We assessed schizotypal traits, using the Schizotypal Personality Questionnaire (SPQ), in a community-based sample of 62 Moroccan migrants and 41 Dutch nonmigrants, who were classified by the presence or absence of a family history of psychopathology. Overall, Moroccan migrants obtained higher SPQ scores than Dutch nonmigrants. However, migrants who had been classified as having a familial load of psychopathology displayed higher SPQ scores than migrants without such a family history, who in turn did not differ from Dutch nonmigrants. Furthermore, migrants with a familial load, relative to migrants without such a family history, reported higher levels of substance use and feelings of anxiety or depression, and perceived more often ethnic discrimination, which closely paralleled their SPQ scores. These findings indicate that primarily those migrants who are both intrinsically vulnerable and chronically exposed to social adversity, particularly ethnic discrimination, are at elevated risk for psychotic and other disorders. The results add to the evidence that migration status and perceived discrimination are associated with mental health.

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          False-positive psychology: undisclosed flexibility in data collection and analysis allows presenting anything as significant.

          In this article, we accomplish two things. First, we show that despite empirical psychologists' nominal endorsement of a low rate of false-positive findings (≤ .05), flexibility in data collection, analysis, and reporting dramatically increases actual false-positive rates. In many cases, a researcher is more likely to falsely find evidence that an effect exists than to correctly find evidence that it does not. We present computer simulations and a pair of actual experiments that demonstrate how unacceptably easy it is to accumulate (and report) statistically significant evidence for a false hypothesis. Second, we suggest a simple, low-cost, and straightforwardly effective disclosure-based solution to this problem. The solution involves six concrete requirements for authors and four guidelines for reviewers, all of which impose a minimal burden on the publication process.
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            Schizophrenia genes, gene expression, and neuropathology: on the matter of their convergence.

            This review critically summarizes the neuropathology and genetics of schizophrenia, the relationship between them, and speculates on their functional convergence. The morphological correlates of schizophrenia are subtle, and range from a slight reduction in brain size to localized alterations in the morphology and molecular composition of specific neuronal, synaptic, and glial populations in the hippocampus, dorsolateral prefrontal cortex, and dorsal thalamus. These findings have fostered the view of schizophrenia as a disorder of connectivity and of the synapse. Although attractive, such concepts are vague, and differentiating primary events from epiphenomena has been difficult. A way forward is provided by the recent identification of several putative susceptibility genes (including neuregulin, dysbindin, COMT, DISC1, RGS4, GRM3, and G72). We discuss the evidence for these and other genes, along with what is known of their expression profiles and biological roles in brain and how these may be altered in schizophrenia. The evidence for several of the genes is now strong. However, for none, with the likely exception of COMT, has a causative allele or the mechanism by which it predisposes to schizophrenia been identified. Nevertheless, we speculate that the genes may all converge functionally upon schizophrenia risk via an influence upon synaptic plasticity and the development and stabilization of cortical microcircuitry. NMDA receptor-mediated glutamate transmission may be especially implicated, though there are also direct and indirect links to dopamine and GABA signalling. Hence, there is a correspondence between the putative roles of the genes at the molecular and synaptic levels and the existing understanding of the disorder at the neural systems level. Characterization of a core molecular pathway and a 'genetic cytoarchitecture' would be a profound advance in understanding schizophrenia, and may have equally significant therapeutic implications.
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              Gene-environment interplay and psychopathology: multiple varieties but real effects.

              Gene-environment interplay is a general term that covers several divergent concepts with different meanings and different implications. In this review, we evaluate research evidence on four varieties of gene-environment interplay. First, we consider epigenetic mechanisms by which environmental influences alter the effects of genes. Second, we focus on variations in heritability according to environmental circumstances. Third, we discuss what is known about gene-environment correlations. Finally, we assess concepts and findings on the interaction between specific identified genes and specific measured environmental risks. In order to provide an understanding of what may be involved in gene-environment interplay, we begin our presentation with a brief historical review of prevailing views about the role of genetic and environmental factors in the causation of mental disorders, and we provide a simplified account of some of the key features of how genes 'work'.
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                Author and article information

                Journal
                EJOP
                Eur J Psychol
                Europe's Journal of Psychology
                Eur. J. Psychol.
                PsychOpen
                1841-0413
                30 August 2013
                : 9
                : 3
                : 552-571
                Affiliations
                [a ]Department of Developmental and Clinical Psychology, Tilburg University, Tilburg, The Netherlands
                Author notes
                [* ]Science & Education, P.O. Box 92035, 1090 AA Amsterdam, The Netherlands. ovdstelt@ 123456gmail.com
                Article
                ejop.v9i3.623
                10.5964/ejop.v9i3.623
                d7cb4e0b-2b1f-416a-a43a-5ff2db5b2fbf
                Copyright @

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 03 May 2013
                : 26 June 2013
                Categories
                Research Reports

                Psychology
                mental health,psychotic disorders,ethnic minority,individual differences,perceived discrimination,schizophrenia,high-risk

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