Longitudinal transcriptome-wide gene expression analysis of sleep deprivation treatment shows involvement of circadian genes and immune pathways.

Therapeutic sleep deprivation (SD) rapidly induces robust, transient antidepressant effects in a large proportion of major mood disorder patients suffering from a depressive episode, but underlying biological factors remain poorly understood. Research suggests that these patients may have altered circadian molecular genetic 'clocks' and that SD functions through 'resetting' dysregulated genes; additional factors may be involved, warranting further investigation. Leveraging advances in microarray technology enabling the transcriptome-wide assessment of gene expression, this study aimed to examine gene expression changes accompanying SD and recovery sleep in patients suffering from an episode of depression. Patients (N = 78) and controls (N = 15) underwent SD, with blood taken at the same time of day before SD, after one night of SD and after recovery sleep. A transcriptome-wide gene-by-gene approach was used, with a targeted look also taken at circadian genes. Furthermore, gene set enrichment, and longitudinal gene set analyses including the time point after recovery sleep, were conducted. Circadian genes were significantly affected by SD, with patterns suggesting that molecular clocks of responders and non-responders, as well as patients and controls respond differently to chronobiologic stimuli. Notably, gene set analyses revealed a strong widespread effect of SD on pathways involved in immune function and inflammatory response, such as those involved in cytokine and especially in interleukin signalling. Longitudinal gene set analyses showed that in responders these pathways were upregulated after SD; in non-responders, little response was observed. Our findings emphasize the close relationship between circadian, immune and sleep systems and their link to etiology of depression at the transcriptomic level.

[Validation of a German Adaptation of the Self-Stigma of Depression Scale (SSDS) for Measuring Self-Stigmatization of People with Depression (SSDS-D)]. / Validierung einer deutschen, adaptierten Fassung der Self-Stigma of Depression Scale (SSDS) zur Messung von Selbststigmatisierung bei Personen mit Depression (SSDS-D).

The 16-item Self-Stigma of Depression Scale (SSDS) was developed to measure anticipated self-stigma hypothetically in case of depression. It is perfect for assessing anticipated self-stigma in community samples. However, in clinical samples measuring actual experienced instead of hypothetical self-stigma may be more appropriate. Aims of this study were the adaptation and validation of the SSDS specifically for people with depression. The abbreviation SSDS-D will be used in the following (D for depression) for this adapted version. All 16 items were translated into German and changed into indicative. Factor structure, internal consistency and construct validity were tested in two independent clinical samples (NA=550; NB=180). In sample A, the original structure of four factors (representing Shame, Self-Blame, Help-Seeking Inhibition, and Social Inadequacy) could be replicated in exploratory factor analyses with the exception of one item. In sample B, confirmatory factor analyses indicated a better fit for the empirically derived than for the alternatively tested original factor structure. Internal consistencies of subscales were satisfying to very good. Even controlled for current depressive symptoms, there were significant correlations to self-esteem and other self-stigma scales as expected, supporting the construct validity of SSDS-D. The SSDS-D appears to be a valid and reliable scale covering experienced self-stigma of people with depression. It may be used in clinical samples to identify correlates, test theoretical models and the efficacy of interventions.

Response to therapeutic sleep deprivation: a naturalistic study of clinical and genetic factors and post-treatment depressive symptom trajectory.

Research has shown that therapeutic sleep deprivation (SD) has rapid antidepressant effects in the majority of depressed patients. Investigation of factors preceding and accompanying these effects may facilitate the identification of the underlying biological mechanisms. This exploratory study aimed to examine clinical and genetic factors predicting response to SD and determine the impact of SD on illness course. Mood during SD was also assessed via visual analogue scale. Depressed inpatients (n = 78) and healthy controls (n = 15) underwent ~36 h of SD. Response to SD was defined as a score of ≤ 2 on the Clinical Global Impression Scale for Global Improvement. Depressive symptom trajectories were evaluated for up to a month using self/expert ratings. Impact of genetic burden was calculated using polygenic risk scores for major depressive disorder. In total, 72% of patients responded to SD. Responders and non-responders did not differ in baseline self/expert depression symptom ratings, but mood differed. Response was associated with lower age (p = 0.007) and later age at life-time disease onset (p = 0.003). Higher genetic burden of depression was observed in non-responders than healthy controls. Up to a month post SD, depressive symptoms decreased in both patients groups, but more in responders, in whom effects were sustained. The present findings suggest that re-examining SD with a greater focus on biological mechanisms will lead to better understanding of mechanisms of depression.

[Medial Stigmatization of Mentally Ill Persons after the "Germanwings"-Crash]. / Mediale Stigmatisierung psychisch Kranker im Zuge der "Germanwings"-Katastrophe.

OBJECTIVE: The present study was designed to investigate the frequency of media stigmatization of mentally ill persons after the crash of the "Germanwings"-aircraft on March 2015. METHOD: Evaluation of 251 texts, which were published in 12 national German newspapers. Categorical distinction between risky coverage and explicit characteristics of stigmatization. RESULTS: In 64.1 % of the evaluated texts, a psychiatric disease of the co-pilot was discussed as the possible cause of the crash, making this the most widely-used explanation in the media that we view "risky coverage". Characteristics of explicit stigmatization were found in 31.5 % of the texts. Most prominent category of explicit stigmatization was the rubric "Metaphorical language/dramatizations". It was found in 23.5 % of the articles. CONCLUSION: Predominantly risky coverage of mentally ill persons has occured in the wake of a spectacular crime. By obtaining professional expertise of psychiatrists and consistent interpretation of journalistic guidelines, unintended effects of stigmatization could be avoided in the future.