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Contemporary cognitive models incorporate an information-processing approach in explaining the causes of depression. The common core in these models is that depression is caused by a vicious cycle of negative thoughts and maladaptive behaviours, and maintained by an excessive focus on the causes and consequences of the depression symptoms (i.e. rumination). Using a variety of study designs, this thesis examines three aspects of cognition assumed to underlie this process: negative attentional bias, cognitive control and metacognitions. The thesis shows that using a computerized intervention to target negative attentional bias in currently remitted depression patients leads to reduced interaction between depression and anxiety symptoms, and that this is associated with increased interest and motivation for social involvement. Furthermore, the thesis indicate that there are bidirectional links between depression symptoms, rumination, and negative beliefs about rumination (negative metacognitions) in currently remitted depression patients, suggesting that negative metacognitions have a relevant role in the feedback loop between depression and rumination. The thesis also demonstrates that there is a basic association between negative metacognitions and reduced ability to shift between mental sets, suggesting a fundamental interaction between cognitive control processes and metacognitions. In sum, the findings presented in this thesis are in line with the notion of depression as a complex interplay of several cognitive and emotional mechanisms within and between different levels of processing.

Background: Rumination in response to dysphoric mood heightens the risk of major depressive disorder. Investigating the underlying cognitive mechanism of rumination can lead to a better understanding of the etiology, and development of effective treatment and prevention. Inhibition is important in controlling cognition and behavior. Previous studies have indicated that rumination and inhibition are related in major depressive disorder. This study investigates if reduced effectiveness in inhibiting prepotent responses and elevated rumination can be conceived as etiological factors in major depressive disorder. Method: The data were collected as a part of the project “Cognitive control and serotonergic genes in emotion regulation and depressive rumination". The principal investigator of this project is Martin Aker, and the advisor is Nils Inge Landrø. The author participated in the collection of the data. Participants were 20 formerly depressed and 19 never-depressed females aged 19-63 years old. Prepotent response inhibition was assessed by the Emotional stop-signal task, and rumination was assessed by the Ruminative responses scale. Results: Formerly depressed participants had a statistically significant longer stop-signal reaction time and a statistically significant higher rumination score compared to never-depressed participants. Across the whole sample there was a statistically significant positive correlation between stop-signal reaction times and rumination scores. Conclusion: The present study demonstrates that remitted major depressive disorder is characterized by less effective prepotent response inhibition and elevated rumination, and that less effective prepotent response inhibition is related to elevated rumination. The reciprocal process between inhibition and rumination is discussed and considered a possible etiological mechanism in major depressive disorder.