📋 Browse Articles

Electroconvulsive therapy (ECT) proves to be an effective intervention in severe cases of major depressive disorder (MDD), especially when there is resistance to pharmacological treatment. The neurotrophic hypothesis proposes that an increase in brain-derived neurotrophic factor (BDNF) is one of the mechanisms responsible for the therapeutic response. The aim of this study is to investigate the effects of ECT on peripheral levels of BDNF, measured in serum and plasma, and analyze clinical outcomes associated with this intervention, as well as identify methodological variables that may influence findings. A systematic review and meta-analysis of studies published between 1995 and 2025 on the PubMed, Scopus and Web of Science databases were conducted, following Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines. Studies of BDNF in serum (14) and plasma (6) were performed separately. Clinical effectiveness was evaluated according to average standardized differences in depression scores. Meta-regressions in the R software identified the impact of four moderators: type of ECT, number of sessions, type of anesthetic and the time blood sample was taken. ECT was associated with an increase in BDNF levels in both biological matrices, especially in studies with plasma (I Show less

Treatment-resistant depression (TRD) remains a complex challenge, often requiring interventions beyond standard medications. This review explores factors that may predict positive response to electroconvulsive therapy (ECT), repetitive transcranial magnetic stimulation (rTMS) and ketamine-based treatments to help guide clinical decision-making. A systematic review was conducted following PRISMA 2020 guidelines. English-language, peer-reviewed studies were identified through PubMed, Embase and Google Scholar using search terms such as 'treatment-resistant,' 'outcome,' 'prediction,' 'ECT,' 'rTMS,' and 'ketamine.' Studies were included if they examined clinical, biological or imaging predictors of response in adults with TRD. Case reports, reviews, editorials and non-English articles were excluded. A total of 42 studies were selected from 408 screened. Among these, 23 focused on ketamine/esketamine, 14 on rTMS, and 11 on ECT. Predictive factors were grouped into clinical (e.g., symptom profile, illness duration), biological (e.g., IL-6, CRP, BDNF) and imaging (e.g., cingulate cortex activity, connectivity). Inflammation markers and fronto-limbic network findings appeared across treatments, though findings were inconsistent. While some predictors show promise, clinical use remains limited by methodological differences and small sample sizes. Larger studies are required to identify clinically useful predictors. Additionally, for optimal treatment decision-making, comparative studies are necessary. Show less

Electroconvulsive therapy (ECT) stands as the most effective intervention for treatment-resistant depression; however, its interaction with dietary regulation of the gut-brain axis has not been thoroughly explored. This study aimed to elucidate the mechanistic link between ECT, gut microbiota remodeling, short-chain fatty acid (SCFA) production, and neural plasticity. In this study, mice were subjected to chronic restraint stress (6 h/d for 28 consecutive days) to establish a depression-like model. Utilizing a translational approach that incorporated behavioral assessments, multimodal neuroimaging techniques such as PET-CT and laser speckle contrast imaging, along with multiomics analyses including metagenomics, metabolomics, and transcriptomics in rodent models, we demonstrated that ECT induced significant gut microbiota remodeling, characterized by an enrichment of SCFA-producing genera like Lactobacillus and Bifidobacterium. This remodeling was associated with restored intestinal barrier integrity and elevated plasma SCFA levels. Mechanistically, these microbial metabolites activated hippocampal Wnt/β-catenin signaling pathways, enhancing synaptic plasticity restoration, while concurrent probiotic supplementation further amplified brain-derived neurotrophic factor (BDNF) expression via SCFA-dependent epigenetic mechanisms. Neuroimaging corroborated the normalization of cerebral glucose metabolism and hemodynamic function post-ECT. In conclusion, our findings unveil a novel gut-brain communication pathway by which ECT exerts its antidepressant effects, positioning SCFAs as vital mediators connecting microbial metabolic alterations to neural plasticity. This research not only redefines the role of nutritional biochemistry in neuromodulation but also suggests the potential of microbial metabolite monitoring to tailor antidepressant therapies for enhanced efficacy. Show less