ArticleTranslational psychiatry2025
Genetic and molecular basis of abnormal BOLD signaling variability in patients with major depressive disorder after electroconvulsive therapy.
Article in Translational psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Effects of electroconvulsive therapy on cerebellar-cerebral functional connectivity in patients with treatment-resistant depression and their correlations with gene expression profiles.Psychiatry and clinical neurosciences · 2026Article
- Neurobiological mechanisms of electroconvulsive therapy in major depressive disorder: structure-function coupling with gene expression and molecular mechanism.Translational psychiatry · 2026Article
- Molecular, Structural, and Functional Neuroimaging in Major Depression.Advances in experimental medicine and biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Electroconvulsive therapy (ECT) is an effective and rapid neuromodulatory intervention for treatment-resistant major depressive disorders (MDD). However, the precise mechanisms underlying their efficacies remain unclear. Resting-state functional magnetic resonance imaging (fMRI) data were collected from 84 individuals with MDD and healthy controls before and after ECT, and coefficient of variation of the BOLD signal (CVBOLD) analysis was combined with region of interest (ROI) functional connectivity (FC) analysis. To assess the reliability of the antidepressant mechanism of ECT, we analyzed the changes in CVBOLD in a separate cohort consisting of 35 patients with MDD who underwent ECT. Moreover, transcriptomic and neurotransmitter receptor data were used to reveal the genetic and molecular bases of the changes in CVBOLD. Patients with MDD who underwent ECT demonstrated increased CVBOLD in the left angular cortex and left precuneus. Following ECT, an increase in FC between the left precuneus and right lingual lobes was associated with improvements in Hamilton Depression Rating Scale (HAMD) scores. validation analysis consistently demonstrated similar changes in CVBOLD in two independent cohorts of patients with MDD. Moreover, these changes in CVBOLD were closely associated with thyroid hormone synthesis, oxidative phosphorylation, endocytosis, and the insulin signaling pathway, and were significantly correlated with the receptor/transporter density of serotonin and dopamine. These findings suggest that ECT modulates abnormal functions in the left angular cortex and left precuneus, leading to widespread changes in functional connectivity and neuroplasticity, especially in the default mode network, and exerts an antidepressant effect.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.