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Default mode network connectivity associated with rumination in major depressive disorder: A systematic review of resting-state fMRI studies.

Sep 2026 · Psychiatry research. Neuroimaging · Vol 364, pp. 112332 · 0 citations · 34 references
Medicine

Abstract

Background

Rumination is a central cognitive mechanism in major depressive disorder (MDD) that contributes to symptom persistence, recurrence, and relapse. Although resting-state abnormalities of the default mode network (DMN) are widely reported in depression, it remains unclear which alterations are specifically associated with depressive rumination rather than broader MDD-related dysfunction.

Objective

To synthesise resting-state fMRI evidence on DMN functional connectivity associated with rumination in clinically diagnosed depression.

Methods

A systematic search of PubMed, Embase, and Cochrane databases was conducted in January 2025 in accordance with PRISMA guidelines (PROSPERO: CRD420251104487). Eligible studies included clinically diagnosed MDD, rumination using validated measures, and a healthy control group. Task-based fMRI studies were excluded. Owing to methodological heterogeneity, findings were synthesised narratively.

Results

Twelve studies comprising 314 depressed individuals and 308 controls met inclusion criteria. Rumination was associated with a distinct DMN-centred resting-state profile involving increased anterior DMN connectivity, altered connectivity between DMN subsystems, interactions between DMN regions and frontal-control or salience networks, and increased engagement of DMN-related functional states. Dynamic findings linked rumination to greater DMN-state entries, increased synchrony, and reduced metastability. Several abnormalities observed in MDD, including reduced posterior DMN connectivity, mPFC-parahippocampal and mPFC-PCC variability, were not consistently associated with rumination.

Conclusion

Rumination in clinically diagnosed depression is associated with a distinct DMN-centred resting-state connectivity profile rather than the broader pattern of DMN abnormalities observed in MDD. These findings may help refine neurobiological models of rumination in depression and identify connectivity markers relevant to symptom persistence, relapse risk, and treatment response.

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