Intra- and Inter-Network connectivity of the default mode network differentiates Treatment-Resistant depression from
Ana Rita Barreiros1, Isabella A Breukelaar2, Amourie Prentice3
1Brain Dynamics Centre, Westmead Institute for Medical Research, Sydney, Australia; Westmead Clinical School, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia; School of Clinical Medicine, Faculty of Medicine and Health, University of New South Wales, Sydney, Australia; The Black Dog Institute, Sydney, Australia.
Neuroimage. Clinical
|August 24, 2024
Summary
Investigating neural features in depression reveals altered default mode network (DMN) connectivity in treatment-resistant depression (TRD). Specific anterior cingulate cortex (ACC) hyperconnectivity distinguishes TRD, offering insights into treatment non-responsiveness.
Area of Science:
- Neuroscience
- Psychiatry
- Medical Imaging
Background:
- Depression treatment resistance is a significant clinical challenge.
- Abnormalities in the anterior cingulate cortex (ACC), part of the default mode network (DMN), are implicated in treatment-resistant depression (TRD).
- A gap exists in understanding how DMN connectivity differentiates TRD from treatment-sensitive depression (TSD).
Purpose of the Study:
- To investigate resting-state functional connectivity (rsFC) between the ACC and DMN regions in TRD.
- To elucidate the role of ACC-DMN interactions in the pathophysiology of depression treatment resistance.
- To compare neural network connectivity in TRD, TSD, and healthy controls (HC).
Main Methods:
- Resting-state functional MRI was conducted on 35 TRD patients, 35 TSD patients, and 38 HC.
- Seed-based functional connectivity analyses focused on two ACC subregions (sgACC, rACC) and DMN.
- Independent component analyses (ICA) explored inter-network connectivity of the DMN.
Main Results:
- TRD patients exhibited hyperconnectivity between the rostral ACC (rACC) and the posterior cingulate cortex compared to TSD and HC.
- ICA revealed distinct DMN connectivity patterns in TRD, including altered connections with the visual network and a parietal DMN region.
- These findings differentiate TRD from TSD based on DMN functional connectivity.
Conclusions:
- Confirms hyperconnectivity within the DMN as a neural mechanism in TRD.
- Suggests altered interactions between the DMN and other neural networks contribute to treatment non-responsiveness in depression.
- Highlights the potential of ACC-DMN connectivity as a biomarker for depression treatment outcomes.
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