Introduction There are reports of an increase in depressive symptoms and fear during the COVID-19 pandemic, in particular in patients with depression. This study investigates factors related to fear of COVID-19 in former inpatients suffering from depression and healthy controls by assessing variables typically associated with depression and anxiety disorders, i.e. stressful life events (SLEs), the primary emotions SADNESS, PLAY and SEEKING as well as dysfunctional emotion regulation strategies with respect to suppression and reappraisal. Methods Data of n = 44 former inpatients suffering from depression and n = 49 healthy controls were collected. The study had a longitudinal design with two measurement points. Before the pandemic, SLEs, primary emotions, emotion regulation and depression severity were assessed. During the pandemic, COVID-19 associated stressors and life events, emotion regulation, depression severity and fear of COVID-19 were assessed. Results Fear of COVID-19 and depression severity during the pandemic were significantly higher in former inpatients than in healthy controls. Depression diagnosis, SLEs and depression severity before the pandemic were significant positive predictors of fear of COVID-19. The primary emotion PLAY was a significant negative predictor of fear of COVID-19. Depression severity did not change significantly in healthy controls. Conclusion The results show that risk factors for depression might be risk factors for high fear of COVID-19. In addition, a playful personality could help preventing mental stress in pandemic situations. Thus, positivity based interventions could counteract elevated fear scores during a pandemic.

Automatic semantic processing can be assessed using semantic priming paradigms. Individual differences in semantic priming have been associated with differences in executive functions. The brain-derived neurotrophic factor (BDNF) Val66Met (substitution of valine (Val) to methionine (Met) at codon 66) polymorphism has been shown to be associated with executive functions as well as depression. Depression-associated variables such as depressed mood also moderated the relationship between BDNF Val66Met and executive functions in previous work. In this study, we therefore aimed at investigating whether BDNF Val66Met genotype modulates masked and unmasked semantic priming as well as executive functions and whether sadness is a moderator of these associations. We collected data of N = 155 participants measuring reaction times (RTs) as well as error rates (ERs) in masked and unmasked semantic priming paradigms using a lexical decision task. We assessed the primary emotion of SADNESS using the Affective Neuroscience Personality Scale (ANPS) and working memory using digit span forward and backward tasks. Met+ carriers showed reduced RT priming and increased ER priming in the masked priming paradigm. Even though there was no direct association between BDNF Val66Met and executive functions, SADNESS significantly moderated the association between BDNF Val66Met and executive functions as well as masked RT priming. We suggest that Met+ individuals with low depressive tendencies have not only superior EF, but also a faster and more superficial processing style, compared with Val/Val homozygotes. However, in Met+ individuals, cognitive functioning exhibits a greater vulnerability to depressed emotionality compared with Val/Val homozygotes. Our study thus demonstrates how emotional and molecular genetic factors exert an interacting influence on higher-level cognition.

Automatic and strategic processes in semantic priming can be investigated with masked and unmasked priming tasks. Unmasked priming is thought to enable strategic processes due to the conscious processing of primes, while masked priming exclusively depends on automatic processes due to the invisibility of the prime. Besides task properties, interindividual differences may alter priming effects. In a recent study, masked and unmasked priming based on mean response time (RT) and error rate (ER) differed as a function of the BDNF Val66Met polymorphism (Sanwald et al., 2020). The BDNF Val66Met polymorphism is related to the integrity of several cognitive executive functions and might thus influence the magnitude of priming. In the present study, we reanalyzed this data with drift-diffusion models. Drift-diffusion models conjointly analyze single trial RT and ER data and serve as a framework to elucidate cognitive processes underlying priming. Masked and unmasked priming effects were observed for the drift rates ν, presumably reflecting semantic preactivation. Priming effects on nondecision time t0 were especially pronounced in unmasked priming, suggesting additional conscious processes to be involved in the t0 modulation. Priming effects on the decision thresholds a may reflect a speed-accuracy tradeoff. Considering the BDNF Val66Met polymorphism, we found lowered drift rates and decision thresholds for Met allele carriers, possibly reflecting a superficial processing style in Met allele carriers. The present study shows that differences in cognitive tasks between genetic groups can be elucidated using drift-diffusion modeling.

Background An early onset of depression is associated with higher chronicity and disability, more stressful life events (SLEs), higher negative emotionality as described by the primary emotion SADNESS and more severe depressive symptomatology compared to depression onset later in life. Additionally, methylation of the serotonin transporter gene (SLC6A4) is associated with SLEs and depressive symptoms. Methods We investigated the relation of SLEs, SLC6A4 methylation in peripheral blood, the primary emotions SADNESS and SEEKING (measured by the Affective Neuroscience Personality Scales) as well as depressive symptom severity to age at depression onset in a sample of N = 146 inpatients suffering from major depression. Results Depressed women showed higher SADNESS (t (91.05) = − 3.17, p = 0.028, d = − 0.57) and higher SLC6A4 methylation (t (88.79) = − 2.95, p = 0.02, d = − 0.55) compared to men. There were associations between SLEs, primary emotions and depression severity, which partly differed between women and men. The Akaike information criterion (AIC) indicated the selection of a model including sex, SLEs, SEEKING and SADNESS for the prediction of age at depression onset. SLC6A4 methylation was not related to depression severity, age at depression onset or SLEs in the entire group, but positively related to depression severity in women. Conclusions Taken together, we provide further evidence that age at depression onset is associated with SLEs, personality and depression severity. However, we found no associations between age at onset and SLC6A4 methylation. The joint investigation of variables originating in biology, psychology and psychiatry could make an important contribution to understanding the development of depressive disorders by elucidating potential subtypes of depression.

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