Neural correlates of successful psychotherapy of depression in adolescents

Straub, Joana; Plener, Paul L.; Sproeber, Nina; Sprenger, Linda; Koelch, Michael; Groen, Georg; Abler, Birgit

doi:10.1016/j.jad.2015.05.020

Cited by 48 publications

(26 citation statements)

References 49 publications

(73 reference statements)

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“…Nevertheless, the sample size of this study is comparable to previous studies of psychotherapy-related neurofunctional changes in depression, including the studies by Dichter (2009) andStraub (2015). Secondly, the current study did not include a waiting-list subthreshold depression group as an untreated comparison group.…”

Section: Discussionmentioning

confidence: 52%

Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task

Mori

Okamoto

Okada

et al. 2016

Journal of Affective Disorders

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Section: Discussionmentioning

confidence: 52%

Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task

Mori

Okamoto

Okada

et al. 2016

Journal of Affective Disorders

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“…Normalization of amygdala activation to emotional stimuli has also been associated with successful pharmacological and psychotherapeutic interventions for depression in both adults (Arnone et al, 2012; Fu et al, 2008; Godlewska et al, 2012; Sheline et al, 2001) and adolescents (Straub et al, 2015; Tao et al, 2012). In resting-state functional connectivity (RSFC) studies, reduced amygdala connectivity with the ventral frontal cortex has been observed in depressed adults (Tang et al, 2013; Veer et al, 2010), greater positive amygdala RSFC with the DLPFC has been observed in depressed adolescents relative to healthy controls (Pannekoek et al, 2014), and reduced amygdala RSFC with hippocampus and parahippocampus has been associated with greater depression symptom severity in depressed adolescents (Cullen et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Resting-state functional connectivity of the amygdala and longitudinal changes in depression severity in adolescent depression

Connolly

Blom

et al. 2017

Journal of Affective Disorders

119

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Background The incidence of major depressive disorder (MDD) rises during adolescence, yet the neural mechanisms of MDD during this key developmental period are unclear. Altered amygdala resting-state functional connectivity (RSFC) has been associated with both adolescent and adult MDD, as well as symptom improvement in response to treatment in adults. However, no study to date has examined whether amygdala RSFC is associated with changes in depressive symptom severity in adolescents. Method We examined group differences in amygdala RSFC between medication-naïve depressed adolescents (N=48) and well-matched healthy controls (N=53) cross-sectionally. We then longitudinally examined whether baseline amygdala RSFC was associated with change in depression symptoms three months later in a subset of the MDD group (N=24). Results Compared to healthy controls, depressed adolescents showed reduced amygdala-based RSFC with the dorsolateral prefrontal cortex (DLPFC) and the ventromedial prefrontal cortex (VMPFC). Within the depressed group, more positive baseline RSFC between the amygdala and insulae was associated with greater reduction in depression symptoms three months later. Limitations Only a subset of depressed participants was assessed at follow-up and treatment type and delivery were not standardized. Conclusions Adolescent depression may be characterized by dysfunction of frontolimbic circuits (amygdala-DLPFC, amygdala-VMPFC) underpinning emotional regulation, whereas those circuits (amygdala-insula) subserving affective integration may index changes in depression symptom severity and may therefore potentially serve as a candidate biomarker for treatment response. Furthermore, these results suggest that the biomarkers of MDD presence are distinct from those associated with change in depression symptoms over time.

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“…Second, it has been shown that the intake of epigenetic modifying medicaments like citalopram increases peripheral BDNF levels (Lopez et al, ) which goes along with reduced amygdala reactivity (Murphy, Norbury, O'Sullivan, Cowen, & Harmer, ). Third, a reduction of BDNF methylation could be achieved by psychotherapy (Perroud et al, ), which also results in decreased amygdala reactivity (Straub et al, ). Since altered amygdala reactivity has multiple times been associated with psychiatric disorders (Gaffrey et al, ; Goodman et al, ; Schneider et al, ; Schumann, Bauman, & Amaral, ), our data suggests high BDNF exon IX methylation as a potential risk factor for psychiatric disorders.…”

Section: Discussionmentioning

confidence: 99%

The role of BDNF methylation and Val⁶⁶Met in amygdala reactivity during emotion processing

Redlich

Schneider

Kerkenberg

et al. 2019

Human Brain Mapping

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Epigenetic alterations of the brain-derived neurotrophic factor (BDNF) gene have been associated with psychiatric disorders in humans and with differences in amygdala BDNF mRNA levels in rodents. This human study aimed to investigate the relationship between the functional BDNF-Val 66 Met polymorphism, its surrounding DNA methylation in BDNF exon IX, amygdala reactivity to emotional faces, and personality traits. Healthy controls (HC, n = 189) underwent functional MRI during an emotional face-matching task. Harm avoidance, novelty seeking and reward dependence were measured using the Tridimensional Personality Questionnaire (TPQ). Individual BDNF methylation profiles were ascertained and associated with several BDNF single nucleotide polymorphisms surrounding the BDNF-Val 66 Met, amygdala reactivity, novelty seeking and harm avoidance. Higher BDNF methylation was associated with higher amygdala reactivity (x = 34, y = 0, z = −26, t (166) = 3.00, TFCE = 42.39, p (FWE) = .045), whereby the BDNF-Val 66 Met genotype per se did not show any significant association with brain function. Furthermore, novelty seeking was negatively associated with BDNF methylation (r = −.19, p = .015) and amygdala reactivity (r = −.17, p = .028), while harm avoidance showed a trend for a positive association with BDNF † These authors contributed equally as joint first authors. ‡ These authors contributed equally as joint senior authors.

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Neural correlates of successful psychotherapy of depression in adolescents

Cited by 48 publications

References 49 publications

Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task

Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task

Resting-state functional connectivity of the amygdala and longitudinal changes in depression severity in adolescent depression

The role of BDNF methylation and Val⁶⁶Met in amygdala reactivity during emotion processing

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Neural correlates of successful psychotherapy of depression in adolescents

Cited by 48 publications

References 49 publications

Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task

Behavioral activation can normalize neural hypoactivation in subthreshold depression during a monetary incentive delay task

Resting-state functional connectivity of the amygdala and longitudinal changes in depression severity in adolescent depression

The role of BDNF methylation and Val66Met in amygdala reactivity during emotion processing

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The role of BDNF methylation and Val⁶⁶Met in amygdala reactivity during emotion processing