Antistigma campaigns have been promoting a medical view of schizophrenia. Given the growing body of research finding negative associations between biogenetic (BG) causal attributions and stigmatizing attitudes, this approach must be reappraised. The present study investigates the impact of different psychoeducational interventions on the etiology of schizophrenia (BG and psychosocial [PS], vs a neutral condition) and on stigmatizing attitudes in medical (n = 60) and psychology students (n = 61). Information was presented via information brochures and a video presentation. Attitudes were assessed before and after the interventions on an explicit level using the stereotype questionnaire and the Social Distance Scale as well as on an implicit level, using the Implicit Association Test. Both educational interventions produced a significant decrease in several stereotype components, which was not the case in the neutral condition. The BG intervention decreased the attribution of blame in both groups. It also decreased the stereotype unpredictability/incompetence and social distance in the medical students but increased the negative outlook on prognosis in the psychology students. The PS intervention reduced the widespread stereotype of dangerousness as well as social distance in the group of medical students. While further research into antistigma interventions is necessary, the proposal for antistigma campaigns is to take a multidimensional and balanced approach, which is adapted to target groups and provides additional facts that challenge the myths maintaining stigma.

Novel tools for data-evaluation from gene-expression arrays allow analyses of biochemical pathways which may be influenced by treatment with epigenetic drugs which have originally been designed for re-activation of so-called tumour-suppressor genes that are known as key-molecules regulating differentiation or cell death in malignancy. Considering the fact that these processes are tightly associated with energy metabolism, this study evaluated the expression signature of prominently regulated pathways in the KG-1-leukemia cell line: Following a 3-day incubation, effects of pharmacologic concentrations from the histone-deacetylase inhibitor SAHA (suberoyl anilide hydroxamic acid, vorinostat) and the methylation-inhibitor desoxy-azacytidine (DAC) were comparatively analysed by transcriptional profiling (based on Affymetrix Human GeneChip Gene 1.0 ST microarrays) and quantitative real time PCR. Expression factors for pathways were calculated for comparative analyses. Epigenetic drugs SAHA and DAC had a downregulatory effect on metabolic pathway factors of carbohydrate metabolism and mitochondrial beta oxidation. Our data confirm SAHA-mediated downregulation of the histone deacetylase SIRT which regulates AKT-phosphatase. Associated pathways lead to regulation of numerous genes, including an upregulation of FOXO transcription factors. These regulatory networks are known for their crucial role in stem cell homeostasis and provide a mechanistic explanation for the fact that the number of SAHA-targeted genes (1392 up, 2651 down) exceeds the number of DAC-targeted genes (60 up, 15 down), besides known effects on cell-cycle-arrest and apoptosis induced by both drugs.Thus, our data underline that epigenetic mechanisms are tightly associated with malignancy-associated metabolic control at least at 3 levels, starting from (i) glucose-uptake over (ii) mitochondrial pathways to (iii) AKT-PTEN-FOXOsignalling. All of them are known to be regulated by caloric restriction. We propose that these interactions should be carefully considered in clinical application, providing the basis for optimization of drug-combinations and complex treatment strategies.

Hohe Vulnerabilität für Diabetes mellitus Fragestellung: Es handelt sich um eine Metaanalyse zur Frage, ob ersterkrankte Schizophreniepatienten bereits Veränderun-gen des Glukosestowechsels aufweisen. Hintergrund: Schizophrenie ist mit einem erhöhten Risiko für das Aureten von Typ-2-Diabetes assoziiert. Bisher ist nicht ein-deutig geklärt, ob dies eine Folge der Erkrankung selbst oder der Behandlung ist, da vor allem atypische Antipsychotika ein metabolisches Syndrom und einen Diabetes induzieren können.

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