Depression: A change of mind

Anthes, Emily

doi:10.1038/515185a

Cited by 59 publications

(28 citation statements)

References 10 publications

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“…For instance, in cognitive-behavioral therapy, patients are given explicit instructions on how to regulate their negative thoughts and emotions, which may increase CEN activity and decrease DMN activity, and thereby enhance patients’ ability to complete reflective processing successfully. 137 – 139 Moreover, mindfulness therapy, which highlights present-moment awareness and acceptance, may alter activity in the SN, especially anterior insular activity, by decreasing the incongruence between the outcome of associative processing and the individual’s expectations. 140 , 141 Based on a meta-analysis, Ma 124 further proposed that antidepressant medication and cognitive-behavioral therapy have different neuropsychological mechanisms: the latter targets prefrontal function by increasing inhibitory executive control, whereas the former may act more directly on the network associated with abnormal emotion generation/experience.…”

Section: Discussionmentioning

confidence: 99%

Cognitive Vulnerability to Major Depression

Wang

Öngür

Auerbach

et al. 2016

Harvard Review of Psychiatry

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Although it is generally accepted that cognitive factors contribute to the pathogenesis of major depressive disorder (MDD), there are missing links between behavioral and biological models of depression. Nevertheless, research employing neuroimaging technologies has provided some elucidation of neurobiological mechanisms related to cognitive vulnerability factors, especially from a whole-brain dynamic perspective. In this review, we integrated well-established MDD cognitive vulnerability factors and corresponding neural mechanism in intrinsic networks under a dual-process framework. We propose that the dynamic alteration and imbalance among the intrinsic networks, both in the resting-state and the rest-task transition stages, contribute to the development of cognitive vulnerability and MDD. Specifically, we propose that abnormally increased resting-state default mode network (DMN) activity and connectivity (mainly in anterior DMN regions) contributes to the foundation of cognitive vulnerability. Furthermore, in the period of rest-to-task transition when subjects confront negative stimuli, the following three kinds of aberrant network interactions have been identified as facilitators of vulnerability and dysphoric mood through different cognitive mechanisms: DMN dominance over the central executive network (CEN), an impaired salience network (SN)-mediated switching between DMN and CEN, and ineffective CEN modulation of the DMN. Focus on interrelated networks and brain activity changes between rest and task states provides a neural-system perspective for future research on depressive vulnerability and resilience, and potentially may guide the development of new intervention strategies for MDD.

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Section: Discussionmentioning

confidence: 99%

Cognitive Vulnerability to Major Depression

Wang

Öngür

Auerbach

et al. 2016

Harvard Review of Psychiatry

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“…As a pivotal component of the affective network (AN), the amygdala has been highlighted in the pathology of MDD [ 2 , 3 ]. This structure is a hub in a wide range of emotion processing, including emotional perception, memory and regulation [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Abnormal amygdala resting-state functional connectivity in adults and adolescents with major depressive disorder: A comparative meta-analysis

et al. 2018

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BackgroundAlthough dysfunction of amygdala-related circuits is centrally implicated in major depressive disorder (MDD), little is known about how this dysfunction differs between adult and adolescent MDD patients.MethodsVoxel-wise meta-analyses of abnormal amygdala resting-state functional connectivity (rsFC) were conducted in adult and adolescent groups separately, followed by a quantitative meta-analytic comparison of the two groups.FindingsNineteen studies that included 665 MDD patients (392 adults and 273 adolescents) and 546 controls (341 adults and 205 adolescents) were identified in the current study. Adult-specific abnormal amygdala rsFC in MDD patients compared to that in controls was located mainly within the affective network, including increased connectivity with the right hippocampus/parahippocampus and bilateral ventromedial orbitofrontal cortex and decreased connectivity with the bilateral insula and the left caudate. Adolescent MDD patients specifically demonstrated decreased amygdala rsFC within the cognitive control network encompassing the left dorsolateral prefrontal cortex and imbalanced amygdala rsFC within the default mode network, which was manifested as hyperconnectivity in the right precuneus and hypoconnectivity in the right inferior temporal gyrus. Additionally, direct comparison between the two groups showed that adult patients had strengthened amygdala rsFC with the right hippocampus/parahippocampus as well as the right inferior temporal gyrus and weakened amygdala rsFC with the bilateral insula compared to that in adolescent patients.InterpretationDistinct impairments of amygdala-centered rsFC in adult and adolescent patients were related to different network dysfunctions in MDD. Adult-specific amygdala rsFC dysfunction within the affective network presumably reflects emotional dysregulation in MDD, whereas adolescent-specific amygdala rsFC abnormalities in networks involved in cognitive control might reflect the neural basis of affective cognition deficiency that is characteristic of adolescent MDD.FundThis study was supported by a grant from the National Natural Science Foundation of China (81671669) and by a Sichuan Provincial Youth Grant (2017JQ0001).

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“…Major depressive disorder (MDD) is a common, diverse, widespread, and intermittent neuropsychiatric burden that includes the wide range of symptoms, such as inability to feel pleasure, lack of motivation, retraction from social interaction, cognitive difficulties, and changes in appetite. 1,2 Depression affects a significant portion of the world's population annually; according to the World Health Organization, it is the leading cause of disability in the world. 3 Extensive research efforts have been done in past decades; however, the etiology of depression is still indefinable, its diagnosis unclear, and the pharmacotherapy ineffective.…”

Section: Introductionmentioning

confidence: 99%

<p>Identification of key genes, pathways and miRNA/mRNA regulatory networks of CUMS-induced depression in nucleus accumbens by integrated bioinformatics analysis</p>

Zhang

Wei

et al. 2019

NDT

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Introduction: Major depressive disorder (MDD) is a recurrent, devastating mental disorder, which affects .350 million people worldwide, and exerts substantial public health and financial costs to society. Thus, there is a significant need to discover innovative therapeutics to treat depression efficiently. Stress-induced dysfunction in the subtype of neuronal cells and the change of synaptic plasticity and structural plasticity of nucleus accumbens (NAc) are implicated in depression symptomology. However, the molecular and epigenetic mechanisms and stresses to the NAc pathological changes in depression remain elusive. Materials and methods: In this study, treatment group mice were treated continually with the chronic unpredictable mild stress (CUMS) until expression of depression-like behaviors were found. Depression was confirmed with sucrose preference, novelty-suppressed feeding, forced swimming, and tail suspension tests. We applied high-throughput RNA sequencing to assess microRNA expression and transcriptional profiles in the NAc tissue from depression-like behaviors mice and control mice. The regulatory network of miRNAs/mRNAs was constructed based on the high-throughput RNA sequence and bioinformatics software predictions. Results: A total of 17 miRNAs and 10 mRNAs were significantly upregulated in the NAc of CUMS-induced mice with depression-like behaviors, and 12 miRNAs and 29 mRNAs were downregulated. A series of bioinformatics analyses showed that these altered miRNAs predicted target mRNA and differentially expressed mRNAs were significantly enriched in the MAPK signaling pathway, GABAergic synapse, dopaminergic synapse, cytokine-cytokine receptor interaction, axon guidance, regulation of autophagy, and so on. Furthermore, dual luciferase report assay and qRT-PCR results validated the miRNA/mRNA regulatory network. Conclusion: The deteriorations of GABAergic synapses, dopaminergic synapses, neurotransmitter synthesis, as well as autophagy-associated apoptotic pathway are associated with the molecular pathological mechanism of CUMS-induced depression.

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Depression: A change of mind

Cited by 59 publications

References 10 publications

Cognitive Vulnerability to Major Depression

Cognitive Vulnerability to Major Depression

Abnormal amygdala resting-state functional connectivity in adults and adolescents with major depressive disorder: A comparative meta-analysis

<p>Identification of key genes, pathways and miRNA/mRNA regulatory networks of CUMS-induced depression in nucleus accumbens by integrated bioinformatics analysis</p>

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