This study focuses on the neurobiological changes in MDD patients with high suicidal risk during rapid antidepressant treatments, such as Esketamine and Electroconvulsive Therapy (ECT). Core ObjectivesEstablish a standardized longitudinal cohort for high-risk suicidal populations to ensure high-quality data for clinical transformation. Investigate the biological mechanisms of rapid-acting interventions by analyzing changes in brain function and molecular pathways. Develop predictive biomarkers to identify treatment responders early, thereby reducing ineffective trial-and-error treatments and lowering suicide risk. Methodology \& Data CollectionThe study integrates multi-dimensional data across three critical time points: T0 (Baseline), T1 (Acute Phase/24h post-first treatment), and T2 (Remission Phase/4-6 weeks). Sample Cohort: A total of 130 participants (70 ECT, 30 Esketamine, 30 conventional medication). Multimodal Data Integration:Clinical Phenotyping: Standardized scales including HAMD-17 (Primary Indicator), C-SSRS (Suicide Assessment), and QIDS-SR16. Biological Omics: Whole Genome Sequencing (WGS), single-cell sequencing, proteomics, metabolomics, DNA methylomics, and gut metagenomics. Neuroimaging \& Physiology: Functional MRI (fMRI), Diffusion Tensor Imaging (DTI), and 32-channel resting-state EEG. SignificanceBy capturing dynamic "treatment-response" trajectories, the project aims to move beyond descriptive symptoms to a system biology-based diagnosis. The findings are expected to provide scientific evidence for individualized intervention strategies and improve the efficiency of care for patients with treatment-resistant depression and acute suicidal ideation.
Study Type
OBSERVATIONAL
Enrollment
130
It does not interfere with specific clinical treatment decisions but observes patients under different treatment paths: ECT, Esketamine nasal spray, or conventional antidepressants.
Change in the total score of the Hamilton Depression Rating Scale (HAMD-17) from baseline to follow-up.
Time frame: From enrollment to the end of treatment at 8 weeks
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