Neural systems approaches to understanding major depressive disorder: An intrinsic functional organization perspective

Hamilton, J. Paul; Chen, Michael C.; Gotlib, Ian H.

doi:10.1016/j.nbd.2012.01.015

Cited by 275 publications

(213 citation statements)

References 80 publications

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“…Investigating more basic processes one by one, rather than taking into account an entire and complex syndrome, could indeed enhance understanding of the mechanisms that are crucial in pathological phenotypes, such as the interplay with other networks (Hamilton et al, 2012;Menon, 2011).…”

Section: Conclusion and Future Researchmentioning

confidence: 99%

The Default Mode Network and Recurrent Depression: A Neurobiological Model of Cognitive Risk Factors

et al. 2012

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A neurobiological account of cognitive vulnerability for recurrent depression is presented based on recent developments of resting state neural networks. We propose that alterations in the interplay between task positive (TP) and task negative (TN) elements of the Default Mode Network (DMN) act as a neurobiological risk factor for recurrent depression mediated by cognitive mechanisms. In the framework, depression is characterized by an imbalance between TN-TP components leading to an overpowering of TP by TN activity. The TN-TP imbalance is associated with a dysfunctional internally-focused cognitive style as well as a failure to attenuate TN activity in the transition from rest to task. Thus we propose the TN-TP imbalance as overarching neural mechanism involved in crucial cognitive risk factors for recurrent depression, namely rumination, impaired attentional control, and cognitive reactivity. During remission the TN-TP imbalance persists predisposing to vulnerability of recurrent depression. Empirical data to support this model is reviewed. Finally, we specify how this framework can guide future research efforts.

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Section: Conclusion and Future Researchmentioning

confidence: 99%

The Default Mode Network and Recurrent Depression: A Neurobiological Model of Cognitive Risk Factors

et al. 2012

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“…Major depression is presumably caused by chronic stress life plus genetic vulnerability, and is characterized by persistent negative mood, such as anhedonia, interest loss, and low self‐esteem (Camp & Cannon‐Albright, 2005; Hamilton, Chen, & Gotlib, 2013; Jabbi, Korf, Ormel, Kema, & den Boer, 2008; Keers & Uher, 2012; Klengel & Binder, 2013; Lohoff, 2010; Moylan, Maes, Wray, & Berk, 2013; Wilde, Mitchell, Meiser, & Schofield, 2013). Pathological changes in monoamine synapses, hypothalamus‐pituitary‐adrenal axis, and brain‐derived neurotrophic factor are believed to cause neuronal atrophy in the ventral tegmental area, nucleus accumbens, and prefrontal cortex from depressive patients and depression‐like animals (Banasr, Dwyer, & Duman, 2011; Bennett et al, 2008; Duman, 2010; Elizalde et al, 2008; Ma, Xu, et al, 2016; Pittenger & Duman, 2008; Sandi & Haller, 2015; Xu, Cui, & Wang, 2016).…”

Section: Introductionmentioning

confidence: 99%

microRNA and mRNA profiles in nucleus accumbens underlying depression versus resilience in response to chronic stress

Song

Sun

et al. 2018

American J of Med Genetics Pt B

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Major depression in negative mood is presumably induced by chronic stress with lack of reward. However, most individuals who experience chronic stress demonstrate resilience. Molecular mechanisms underlying stress‐ induced depression versus resilience remain unknown, which are investigated in brain reward circuits. Mice were treated by chronic unpredictable mild stress (CUMS) for 4 weeks. The tests of sucrose preference, Y‐maze, and forced swimming were used to identify depression‐like emotion behavior or resilience. High‐throughput sequencing was used to analyze mRNA and miRNA quantity in the nucleus accumbens (NAc) harvested from the mice in the groups of control, CUMS‐induced depression (CUMS‐MDD), and CUMS‐resistance to identify molecular profiles of CUMS‐MDD versus CUMS‐resilience. In data analyses and comparison among three groups, 1.5‐fold ratio in reads per kilo‐base per million reads (RPKM) was set to judge involvements of mRNA and miRNA in CUMS, MDD, or resilience. The downregulations of serotonergic/dopaminergic synapses, MAPK/calcium signaling pathways, and morphine addiction as well as the upregulations of cAMP/PI3K‐Akt signaling pathways and amino acid metabolism are associated with CUMS‐MDD. The downregulations of chemokine signaling pathway, synaptic vesicle cycle, and nicotine addiction as well as the upregulations of calcium signaling pathway and tyrosine metabolism are associated with CUMS‐resilience. The impairments of serotonergic/dopaminergic synapses and PI3K‐Akt/MAPK signaling pathways in the NAc are associated with depression. The upregulation of these entities is associated with resilience. Consistent results from analyzing mRNA/miRNA and using different methods validate our finding and conclusion.

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“…Structural alterations in the prefrontal cortex, particularly the anterior cingulate, and subcortical hippocampal, amygdalar, thalamic, and striatal/ pallidal centers are consistently implicated (Drevets et al, 2008;Lorenzetti et al, 2009;Schmaal et al, 2015). Lesion and functional imaging studies show these regions form networks governing mood regulation, reward sensitivity, and emotion (Koenigs and Grafman, 2009;Ochsner et al, 2012;Hamilton et al, 2013;Korgaonkar et al, 2013). Symptoms of depression such as amotivation, anhedonia, apathy, and rumination are linked to functional disturbances in the ventral striatum/ pallidum specifically (Disner et al, 2011;Ochsner et al, 2012;Kuhn et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Effect of Electroconvulsive Therapy on Striatal Morphometry in Major Depressive Disorder

Wade

Joshi

Njau

et al. 2016

Neuropsychopharmacol

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Patients with major depression show reductions in striatal and paleostriatal volumes. The functional integrity and connectivity of these regions are also shown to change with antidepressant response. Electroconvulsive therapy (ECT) is a robust and rapidly acting treatment for severe depression. However, whether morphological changes in the dorsal and ventral striatum/pallidum relate to or predict therapeutic response to ECT is unknown. Using structural MRI, we assessed cross-sectional effects of diagnosis and longitudinal effects of ECT for volume and surface-based shape metrics of the caudate, putamen, pallidum, and nucleus accumbens in 53 depressed patients (mean age: 44.1 years, 13.8 SD; 52% female) and 33 healthy controls (mean age: 39.3 years, 12.4 SD; 57% female). Patients were assessed before ECT, after their second ECT, and after completing an ECT treatment index. Controls were evaluated at two time points. Support vector machines determined whether morphometric measures at baseline predicted ECT-related clinical response. Patients showed smaller baseline accumbens and pallidal volumes than controls (Po0.05). Increases in left putamen volume (Po0.03) occurred with ECT. Global increases in accumbens volume and local changes in pallidum and caudate volume occurred in patients defined as treatment responders. Morphometric changes were absent across time in controls. Baseline volume and shape metrics predicted overall response to ECT with up to 89% accuracy. Results support that ECT elicits structural plasticity in the dorsal and ventral striatum/pallidum. The morphometry of these structures, forming key components of limbic-cortical-striatal-pallidal-thalamic circuitry involved in mood and emotional regulation, may determine patients likely to benefit from treatment.

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Neural systems approaches to understanding major depressive disorder: An intrinsic functional organization perspective

Cited by 275 publications

References 80 publications

The Default Mode Network and Recurrent Depression: A Neurobiological Model of Cognitive Risk Factors

The Default Mode Network and Recurrent Depression: A Neurobiological Model of Cognitive Risk Factors

microRNA and mRNA profiles in nucleus accumbens underlying depression versus resilience in response to chronic stress

Effect of Electroconvulsive Therapy on Striatal Morphometry in Major Depressive Disorder

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