Restoring Emotion Regulation Networks in Depression Vulnerability

Major Depression Clinical Trial

Official title:

Restoring Emotion Regulation Networks in Depression Vulnerability: An Experimental Study Applying an Attention Bias Modification Procedure

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT02931487
• Other study ID #: HSØ-2015052
• Status: Completed
• Phase: N/A
• Start date: May 2015
• Est. completion date: December 2016

Study information

• Verified date: April 2019
• Source: University of Oslo
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial 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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 134
• Est. completion date: December 2016
• Est. primary completion date: December 2016
• Accepts healthy volunteers: No
• Gender: All
• Age group: 18 Years to 65 Years

Eligibility

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.

Related Conditions & MeSH terms

• Depression
• Depressive Disorder
• Depressive Disorder, Major
• Major Depression

Intervention

Behavioral:
• Attentional Bias Modification
Computerized
• Sham Comparator
Computerized

Locations

Country	Name	City	State
Norway	University of Oslo, Department of Psychology	Oslo

Sponsors (3)

Lead Sponsor	Collaborator
University of Oslo	Oslo University Hospital, University of Oxford

Country where clinical trial is conducted

Norway, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	BOLD response in prefrontal cortical regions	Stronger fMRI BOLD response in prefrontal cortical regions in ABMT compared to neutral AMB placebo condition.	Two weeks after after ABM-training
Secondary	BOLD response within the amygdala	Lower ABM fMRI BOLD response within the amygdala in ABMT compared to neutral ABM placebo condition.	Two weeks after ABM-training
Secondary	DTI	Increased neural integrity as measured by fractional anisotropy values in the uncinate fasciculi (UF) in the active AMBT compared to neutral ABM placebo condition.	Two weeks after ABM-training
Secondary	RSFC	Increased integrity within the attentional networks at rest as measured by independent component analysis (ICA) in ABMT compared to neutral ABM training.	Two weeks after ABM-training
Secondary	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.	The low expressive variant will be associated with more frontal BOLD activation and lower amygdala activation after ABMT	Two weeks after ABM-training
Secondary	BDNF	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.	Two week after ABM-training
Secondary	Serotonergic cumulative genetic score and fMRI	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.	Two weeks after ABM-training
Secondary	Serotonergic cumulative genetic score and morphompetry	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.	Two weeks after ABM-training
Secondary	Serotonergic cumulative genetic score and fMRI and DTI	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.	Two weeks after ABM-training