Skip to content

Restoring Emotion Regulation Networks in Depression Vulnerability

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

Status
Completed
Phases
NA
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT02931487
Enrollment
134
Registered
2016-10-13
Start date
2015-05-31
Completion date
2016-12-31
Last updated
2019-04-30

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Major Depression

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.

Interventions

Computerized

BEHAVIORALSham Comparator

Computerized

Sponsors

Oslo University Hospital
CollaboratorOTHER
University of Oxford
CollaboratorOTHER
University of Oslo
Lead SponsorOTHER

Study design

Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
PREVENTION
Masking
TRIPLE (Subject, Investigator, Outcomes Assessor)

Eligibility

Sex/Gender
ALL
Age
18 Years to 65 Years
Healthy volunteers
No

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.

Design outcomes

Primary

MeasureTime frameDescription
BOLD response in prefrontal cortical regionsTwo weeks after after ABM-trainingStronger fMRI BOLD response in prefrontal cortical regions in ABMT compared to neutral AMB placebo condition.

Secondary

MeasureTime frameDescription
DTITwo weeks after ABM-trainingIncreased neural integrity as measured by fractional anisotropy values in the uncinate fasciculi (UF) in the active AMBT compared to neutral ABM placebo condition.
RSFCTwo weeks after ABM-trainingIncreased integrity within the attentional networks at rest as measured by independent component analysis (ICA) in ABMT compared to neutral ABM training.
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.Two weeks after ABM-trainingThe low expressive variant will be associated with more frontal BOLD activation and lower amygdala activation after ABMT
BOLD response within the amygdalaTwo weeks after ABM-trainingLower ABM fMRI BOLD response within the amygdala in ABMT compared to neutral ABM placebo condition.
Serotonergic cumulative genetic score and fMRITwo weeks after ABM-trainingA 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.
Serotonergic cumulative genetic score and morphompetryTwo weeks after ABM-trainingA 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.
Serotonergic cumulative genetic score and fMRI and DTITwo weeks after ABM-trainingA 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.
BDNFTwo week after ABM-trainingBrain 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.

Countries

Norway

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 22, 2026