A premise for this project is that targeting basic cognitive and neural mechanisms has the potential to translate into new principles for depression treatment and prevention of relapse of depressive episodes. The project is a translational study testing a new computerized method for correcting implicit biases in emotional information processing (Attention Bias Modification; ABM). The neural changes brought about by ABM is also investigated in a subgroup (brain imaging).This is by far the largest study applying this method in the context of depression. A sample of 321 participants were randomized to an active or a control ("placebo") condition in a RCT study and with design and primary and secondary measures pregistered in Clinical Trials. The participants are followed up 3, 6 and 12 months after the intervention.
ABM training led to significantly greater decrease in clinician rated symptoms of depression (Hamilton Rating Scale for Depression) immediately after the two weeks intervention as compared to the control condition. No significant difference between ABM and placebo was found for self-reported symptoms (Beck Depression Inventory-II). ABM induced a change of Attention Bias towards more positive versus neutral stimuli with a more positive bias being associated with greater symptom reduction.
A network analysis has also been conducted which showed that ABM in particular influences the symptom "interest" positively and which is a core symptom of depression.
A sub-sample (n=134) has also been included in a brain imaging study. Task-related fMRI following ABM training has so far not been investigated in depression and the analyses show that ABM training has an effect on brain function within circuitry associated with emotional appraisal and the generation of affective state.
There is a pressing need to improve treatment and secondary prevention of depression and thus clinical trials should focus not only on efficacy, but also on identification of the underlying mechanisms through which treatment operate. Negative affective bias is such a mechanism and can be targeted by the ABM task. Thus, the implication of the current study is that ABM may have practical potential in the treatment of residual depression.
ABM can be implemented relatively quickly and can also be conducted in the subject's home, which is an advantage as it makes it more feasible as a treatment. Another avenue for the future is that by involving "lower-order" and implicit cognitive processes, ABM interventions might be added to other types of intervention and therapy. Furthermore, and importantly, affective bias might be a basic working mechanism for Cognitive Behavioral Therapy and antidepressant medication. Thus, treatment effectiveness should increase if such biases are modified.
Depression (Major Depressive Disorder; MDD) has been dubbed "the common cold among the mental illnesses" and it is also a highly recurrent disorder. Secondary prevention has been identified as a key goal in the long-term management of depression. High rec urrence rate suggests that there are specific vulnerability factors that increase people's risk for developing repeated episodes of the disorder. Preventive strategies should identify and ameliorate these factors to reduce the individual's risk of subsequ ent episodes. Biased attention for emotional stimuli is central to the cognitive model where increased sensitivity to negative cues is believed to fuel the negative thoughts and feelings in depression and play a key role in maintaing the illness. Selectiv e biases in attention can be modified by a simple computerized technique; The Attention Bias Modification Task (ABM). This project aims to investigate whether ABM can reduce surrogate and clinical markers of relapse in a large group highly vulnerable to d epressive episodes. The effects of ABM on three key risk factors for depression will be studied: Emotion dysregulation, cortisol awakening response and residual symptoms. The hypothesis that ABM will reduce subsequent episodes of low mood over the followi ng 12 months in this group in a manner predicted by early changes in these risk factors will be investigated. It will also be tested if such effects in the lab may be dependent on candidate genes which affect serotonin reuptake and which have been implica ted in malleability and emotional learning. Effects on underlying neural correlates of emotion regulation will be studied in an fMRI experiment in a sub-sample stratified by serotonin transporter genotype. The characterisation of the genetic and neural me chanisms underlying the ABM effect will have key implications for future treatment development and combination with other treatment modalities like pharmacotherapy.