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Restoring Emotion Regulation Networks in Depression Vulnerability

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
 
ClinicalTrials.gov Identifier: NCT02931487
Recruitment Status : Completed
First Posted : October 13, 2016
Last Update Posted : April 30, 2019
Sponsor:
Collaborators:
Oslo University Hospital
University of Oxford
Information provided by (Responsible Party):
Nils Inge Landrø, University of Oslo

Brief Summary:
Selective biases in attention can be modified by a simple computerized technique: The Attention Bias Modification Task (ABM) pioneered by MacLeod et al. Cognitive biases may be one reason depression recurs, and altering these biases should reduce risk of recurrence. Recently, evidence has supported this hypothesis . The mechanisms by which ABM works are not well understood. More research is needed to explore how altering an implicit attentional bias can lead to changes in subjective mood. One possible explanation is that positive attentional biases are an important component of explicit methods of emotion regulation. The ability to effectively regulate one's emotions is a fundamental component of mental health and this ability is impaired in depression. It has also been shown that recovered depressed people spontaneously show a more dysfunctional pattern of emotion regulation as compared to never depressed controls. Supporting this, growing evidence implicates dysregulation of a medial/orbitofrontal circuit in mood disorders. This circuit includes the orbitofrontal cortex and anterior cingulate cortex, the ventral striatum, the ventral pallidum and medial thalamus. Components of this circuit are reciprocally connected with the amygdala, which is implicated in emotional processing in the healthy brain and dysregulated in depression. Negative emotion processing biases depend on both enhanced "bottom-up" responses to emotionally salient stimuli and reduces "top-down" cognitive control mechanisms, required to suppress responses to emotionally salient but task irrelevant information. Cognitive reappraisal and distancing are common strategies to down- or upregulate emotional responses. Reappraisal is an emotion regulation strategy that involves reinterpretation and changing the way one thinks about an event or stimulus with the goal of changing its affective impact. Distancing is a type of reappraisal that involves creating mental space between oneself and the emotional event in order to see things from a different, less self-focused perspective. It has been shown that distancing is a strategy that people can improve at over time compared to reinterpretation. The neural systems which support the explicit regulation of emotion have previously been characterized and include both lateral- and prefrontal cortex. This frontal activity is predicted to downregulate limbic circuitry involving the amygdala during passive viewing of emotional salient stimuli.

Condition or disease Intervention/treatment Phase
Major Depression Behavioral: Attentional Bias Modification Behavioral: Sham Comparator Not Applicable

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Study Type : Interventional  (Clinical Trial)
Actual Enrollment : 134 participants
Allocation: Randomized
Intervention Model: Parallel Assignment
Masking: Triple (Participant, Investigator, Outcomes Assessor)
Primary Purpose: Prevention
Official Title: Restoring Emotion Regulation Networks in Depression Vulnerability: An Experimental Study Applying an Attention Bias Modification Procedure
Study Start Date : May 2015
Actual Primary Completion Date : December 2016
Actual Study Completion Date : December 2016

Resource links provided by the National Library of Medicine


Arm Intervention/treatment
Experimental: Attentional Bias Modification
ABM dot-probe task with image stimuli (faces) of three valences: positive (happy), neutral, or negative (angry and fearful). In the ABM condition, probes were located behind positive stimuli in 87 % of the trials (valid trials), as opposed to 13% with probes located behind the more negative stimuli (invalid trials). Consequently, participants should implicitly learn to deploy their attention toward positive stimuli, and in this way develop a more positive AB when completing the task.
Behavioral: Attentional Bias Modification
Computerized

Sham Comparator: Sham comparator
Sham condition without modification of attentional bias. These trials are identical in structure to the ABM trials with the exception that target probes replaced negative and positive images with equal frequency.
Behavioral: Sham Comparator
Computerized




Primary Outcome Measures :
  1. BOLD response in prefrontal cortical regions [ Time Frame: Two weeks after after ABM-training ]
    Stronger fMRI BOLD response in prefrontal cortical regions in ABMT compared to neutral AMB placebo condition.


Secondary Outcome Measures :
  1. BOLD response within the amygdala [ Time Frame: Two weeks after ABM-training ]
    Lower ABM fMRI BOLD response within the amygdala in ABMT compared to neutral ABM placebo condition.

  2. DTI [ Time Frame: Two weeks after ABM-training ]
    Increased neural integrity as measured by fractional anisotropy values in the uncinate fasciculi (UF) in the active AMBT compared to neutral ABM placebo condition.

  3. RSFC [ Time Frame: Two weeks after ABM-training ]
    Increased integrity within the attentional networks at rest as measured by independent component analysis (ICA) in ABMT compared to neutral ABM training.

  4. 5-HTTLPR + A>G polymorphic variation divided by the triallelic functional "high expressive" versus "low expressive" genotype will moderate the impact from ABMT as measured by whole brain BOLD responses. [ Time Frame: Two weeks after ABM-training ]
    The low expressive variant will be associated with more frontal BOLD activation and lower amygdala activation after ABMT

  5. BDNF [ Time Frame: Two week after ABM-training ]
    Brain Derived Neurotropic Factor (BDNF) val66met polymorphic variation linked to Brain Derived Neurotropic Factor (BDNF) variation will differentiate between ABMT and neutral AMB placebo as measured by fMRI whole brain BOLD responses.

  6. Serotonergic cumulative genetic score and fMRI [ Time Frame: Two weeks after ABM-training ]
    A serotonergic cumulative Genetic score, including (5-HHTLPR, HTR1A 8rs6295) and HTR 2A (rs 6311) polymorphisms will moderate the effects of ABM on fMRI BOLD signal compared to a neutral placebo condition.

  7. Serotonergic cumulative genetic score and morphompetry [ Time Frame: Two weeks after ABM-training ]
    A serotonergic cumulative Genetic score, including (5-HHTLPR, HTR1A 8rs6295) and HTR 2A (rs 6311) polymorphisms will moderate the effects of ABM on structural MRI as measured by total grey matter volume compared to a neutral placebo condition.

  8. Serotonergic cumulative genetic score and fMRI and DTI [ Time Frame: Two weeks after ABM-training ]
    A serotonergic cumulative Genetic score, including (5-HHTLPR, HTR1A 8rs6295) and HTR 2A (rs 6311) polymorphisms will moderate the effects of ABM on DTI MRI as measured by fractional anisotropy compared to a neutral placebo condition.



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Ages Eligible for Study:   18 Years to 65 Years   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Criteria

Inclusion Criteria:

  • Currently no-depressed subjects with a history of major depression.

Exclusion Criteria:

  • Current or past neurological illness, bipolar disorder, psychosis or drug addiction.

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02931487


Locations
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Norway
University of Oslo, Department of Psychology
Oslo, Norway, 0317
Sponsors and Collaborators
University of Oslo
Oslo University Hospital
University of Oxford
Investigators
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Principal Investigator: Nils I Landrø, phd University of Oslo
Publications automatically indexed to this study by ClinicalTrials.gov Identifier (NCT Number):
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Responsible Party: Nils Inge Landrø, Professor Dr. philos, University of Oslo
ClinicalTrials.gov Identifier: NCT02931487    
Other Study ID Numbers: HSØ-2015052
First Posted: October 13, 2016    Key Record Dates
Last Update Posted: April 30, 2019
Last Verified: April 2019
Individual Participant Data (IPD) Sharing Statement:
Plan to Share IPD: No
Additional relevant MeSH terms:
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Depression
Depressive Disorder
Behavioral Symptoms
Mood Disorders
Mental Disorders