Neural signatures of default mode network in major depression disorder after electroconvulsive therapy

Cereb Cortex. 2023 Mar 21;33(7):3840-3852. doi: 10.1093/cercor/bhac311.

Abstract

Functional abnormalities of default mode network (DMN) have been well documented in major depressive disorder (MDD). However, the association of DMN functional reorganization with antidepressant treatment and gene expression is unclear. Moreover, whether the functional interactions of DMN could predict treatment efficacy is also unknown. Here, we investigated the link of treatment response with functional alterations of DMN and gene expression with a comparably large sample including 46 individuals with MDD before and after electroconvulsive therapy (ECT) and 46 age- and sex-matched healthy controls. Static and dynamic functional connectivity (dFC) analyses showed increased intrinsic/static but decreased dynamic functional couplings of inter- and intra-subsystems and between nodes of DMN. The changes of static functional connections of DMN were spatially correlated with brain gene expression profiles. Moreover, static and dFC of the DMN before treatment as features could predict depressive symptom improvement following ECT. Taken together, these results shed light on the underlying neural and genetic basis of antidepressant effect of ECT and the intrinsic functional connectivity of DMN have the potential to serve as prognostic biomarkers to guide accurate personalized treatment.

Keywords: default mode network; electroconvulsive therapy; gene expression; major depressive disorder; prediction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antidepressive Agents / therapeutic use
  • Brain / diagnostic imaging
  • Brain Mapping / methods
  • Default Mode Network
  • Depression
  • Depressive Disorder, Major* / drug therapy
  • Depressive Disorder, Major* / therapy
  • Electroconvulsive Therapy*
  • Humans
  • Magnetic Resonance Imaging / methods
  • Neural Pathways / diagnostic imaging

Substances

  • Antidepressive Agents