• Dynamic causal modeling (DCM) applied after rTMS reveals network-level changes in major depressive disorder.1
  • DCM provides mechanistic insight into rTMS effects on depression-relevant circuits.1 1

Weekly enrichment (2026-07-20)

  • The ScienceDirect source article (Journal of Affective Disorders, PII S0165032726001484) did not load during enrichment; a title-based search identified the closest primary source on this exact topic as Kita et al., “Exploring the capabilities of repetitive transcranial magnetic stimulation in major depressive disorder: Dynamic causal modeling of the neural network,” Translational Psychiatry 15, 257 (2025).2 3
  • That study applied dynamic causal modeling to a large-sample, multi-site resting-state fMRI dataset comprising 270 healthy controls and 175 patients with MDD across three imaging sites, with DCM estimated in SPM12.2 3
  • The modeled network centered on the left dorsolateral prefrontal cortex (DLPFC)—the standard rTMS target—together with the amygdala (AMY), nucleus accumbens (NAC), thalamus (Thal), anterior insula (AI), subgenual anterior cingulate cortex (sgACC), ventromedial PFC (VMPFC), and visual cortex (VIS).2
  • In MDD, aberrant causal connections ran from the left DLPFC, amygdala, nucleus accumbens, and thalamus to the visual cortex, implicating VIS in the disorder’s circuitry.2
  • Depression severity was negatively associated with the nucleus accumbens–to–visual cortex connection and positively associated with the amygdala–to–sgACC connection.2
  • Additional aberrant connections linked the VMPFC with the amygdala, nucleus accumbens, and sgACC—consistent with corticostriatal disruption of emotional regulation—alongside decreased self-inhibition within the thalamus.2
  • The authors argue these mapped circuits are candidate nodes that left-DLPFC rTMS may modulate, providing mechanistic rationale for connectivity-informed, personalized treatment; specific effect sizes and stimulation parameters from the original ScienceDirect article could not be verified here.2 3

Footnotes

  1. https://www.sciencedirect.com/science/article/pii/S0165032726001484?dgcid=rss_sd_all 2 3

  2. https://www.nature.com/articles/s41398-025-03480-7 2 3 4 5 6 7

  3. https://doi.org/10.1038/s41398-025-03480-7 2 3