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Background: This study investigates (1) whether alterations in magnetic resonance imaging (MRI)-based structural global network organization is impaired in patients with major depressive disorder (MDD), (2) whether in-patient treatment including pharmacological, psychological and neurostimulation interventions is linked to changes in structural brain connectivity and (3) whether brain structural changes relate to changes in depression symptomatology.
Methods: One hundred seventy-eight subjects – 109 subjects diagnosed with current MDD and 55 healthy controls (HC) - participated in the present study (baseline + 6-weeks follow up). Fifty-six depressed patients were treated with electroconvulsive therapy (ECT) and 67 received in-patient treatment without ECT. Here, grey matter T1-weighted MRI was used to define nodes and DWI-based tractography to define the connections – or edges – between the nodes creating a structural connectome. Changes over time in depressions symptom severity was measured with the Hamilton Depression Ratings Scale.
Results: MDD patients showed reduced connectivity strength at baseline compared to healthy controls. MDD patients showed a significant increase of connectivity strength over time, an effect that was not detected in HC. An increase of connectivity strength was associated with a decrease in depression symptom severity. These effects were independent of treatment choice, suggesting a nonspecific effect that cannot be traced back to ECT.
Conclusion: We demonstrate an alleviation of structural brain dysconnectivity in MDD patients after successful antidepressive treatment, which is most prominent in those patients that show the greatest reduction in depressive symptomatology. This pattern of results suggests neuroplastic mechanisms involved in the successful treatment of depression and should be investigated as a potential treatment target in future studies.
Research Category and Technology and Methods: Clinical Research: 2. Electroconvulsive Therapy (ECT)
Myocardial injury as induced by myocardial infarction results in tissue ischemia, which critically incepts cardiomyocyte death. Endothelial cells play a crucial role in restoring oxygen and nutrient supply to the heart. Latest advances in single-cell multi-omics, together with genetic lineage tracing, reveal a transcriptional and phenotypical adaptation to the injured microenvironment, which includes alterations in metabolic, mesenchymal, hematopoietic and pro-inflammatory signatures. The extent of transition in mesenchymal or hematopoietic cell lineages is still debated, but it is clear that several of the adaptive phenotypical changes are transient and endothelial cells revert back to a naïve cell state after resolution of injury responses. This resilience of endothelial cells to acute stress responses is important for preventing chronic dysfunction. Here, we summarize how endothelial cells adjust to injury and how this dynamic response contributes to repair and regeneration. We will highlight intrinsic and microenvironmental factors that contribute to endothelial cell resilience and may be targetable to maintain a functionally active, healthy microcirculation.