Translational Psychiatry最新文献

{"title":"Microglial deletion induces despair-like behavior associated with astrogliosis.","authors":"Xun Wang, Shi-Han Liao, Nan Wang, Ya-Ting Chen, Rui-Han Huang, Di-Ji Li, Wen-Ying Jiang, Xiao-Wen Li, Tian-Ming Gao, Jian-Ming Yang","doi":"10.1038/s41398-026-04325-7","DOIUrl":"10.1038/s41398-026-04325-7","url":null,"abstract":"<p><p>Microglia, the brain's resident immune cells, are increasingly recognized as key regulators of brain physiology and behavior. However, their specific role in affective states remains controversial, with studies reporting conflicting depression-like outcomes following their removal. Using the colony stimulating factor-1 receptor (CSF1R) inhibitor PLX5622 in adult mice of both sexes, we found that microglial deletion selectively induced despair-like behavior (increased immobility in the forced swim test and the tail suspension test) in either sex, without affecting locomotion, anxiety, sociability, anhedonia, or cognition. This effect was accompanied by reactive astrogliosis in the medial prefrontal cortex (mPFC). Unexpectedly, microglial deletion induced a predominant A2-like astrocyte reactivity. Notably, both the despair-like and A2-like phenotypes resolved upon microglia repopulation. Critically, pharmacological inhibition of these hyperactive mPFC astrocytes with fluorocitrate reversed the despair-like phenotype, indicating that microglial loss triggers maladaptive astrocyte reactivity that drives behavioral despair. Our results reveal an essential role for microglia in maintaining emotional homeostasis, possibly through interaction with astrocytes.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13710846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149273499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Abnormalities of intrinsic brain activity in late-life depression: a meta-analysis of resting-state functional imaging studies.","authors":"Jinping Lin, Lin Lin, Huawei Zhang, Graham J Kemp, Lei Li, Qiyong Gong","doi":"10.1038/s41398-026-04210-3","DOIUrl":"10.1038/s41398-026-04210-3","url":null,"abstract":"<p><p>Neuroimaging studies using a variety of techniques have demonstrated abnormal patterns of spontaneous brain activity in patients with late-life depression (LLD). However, the findings are variable and often inconsistent, hindering understanding of underlying neuropathology. We conducted a meta-analysis of whole-brain resting-state functional neuroimaging studies in LLD compared to healthy controls (HC), using anisotropic effect-size seed-based d mapping, to identify the most consistent brain activity alterations and their relation to clinical features. After systematic literature search, we included 13 studies reporting resting-state functional activity in a total of 476 LLD patients compared with 394 HC. We found higher activity in LLD vs HC in the left fusiform gyrus (FG), right parahippocampal gyrus (PHG) and right middle frontal gyrus (MFG), and lower brain activity in the left supplementary motor area (SMA), left superior frontal gyrus (SFG) and left postcentral gyrus (PoCG). In the subgroup meta-analysis of studies with a single functional index, LLD showed higher regional homogeneity (ReHo) in the left FG and right PHG, and also higher amplitude of low frequency fluctuations and/or fractional amplitude of low frequency fluctuations (ALFF/fALFF) in the left FG and lower activity in the left SFG. In the subgroup meta-analysis of studies using corrected p values, LLD vs HC showed similar patterns, with higher activity in the left FG, right PHG, and right MFG, and lower activity in the left SFG, left superior occipital gyrus (SOG), left PoCG, and left SMA. This study advances understanding of brain resting-state functional imaging features underlying LLD. These findings may have practical implications in the clinical diagnosis of and intervention for LLD.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149138534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Attenuated PER3 amplitude in hair follicles is associated with sleep irregularity in schizophrenia.","authors":"Mikkel E I Kolind, Rikke Kruse, Jan C Brønd, Afsaneh M Nejad, Lasse K Bak, Charlotte S Larsen, Kurt Højlund, Christoph P Beier, Elsebeth Stenager, Claus B Juhl","doi":"10.1038/s41398-026-04295-w","DOIUrl":"10.1038/s41398-026-04295-w","url":null,"abstract":"<p><p>Circadian dysregulation is prevalent in both schizophrenia and obesity, yet the molecular mechanisms underpinning these disturbances remain unclear. We examined circadian variation in clock gene expression using repeated hair follicle self-sampling across two days in 66 adults: 22 with schizophrenia and obesity (SCH-OB), 22 with obesity but no psychiatric disorder (OB), and 22 normal-weight controls (LEAN). Gene expression was quantified by qPCR, and complementary markers included salivary cortisol and melatonin, oral pH and temperature, and accelerometer-derived sleep metrics. Evidence of rhythmic expression was detected in five of six clock genes. PER3 amplitude was significantly reduced in SCH-OB compared with both OB and LEAN (p < 0.01) and correlated positively with sleep regularity (p = 0.006). Cortisol rhythms were preserved across groups, whereas melatonin amplitude was attenuated in SCH-OB relative to LEAN (p < 0.05). Hair follicle sampling proved highly feasible, with >98% compliance. These findings indicate that individuals with schizophrenia exhibit dampened circadian rhythms in PER3 expression that parallel irregular sleep patterns, supporting hair follicle-based sampling as a practical tool for assessing molecular rhythm parameters in real-world conditions.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13710538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149273627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early life adversity shapes neural and behavioural responses to oxytocin during altruistic decision-making.","authors":"Nina Marsh, Vanessa Jeske, Mari Babasiz, Angela Herscheid, Ann-Kathrin Kreuder, Rüdiger Stirnberg, Tony Stoecker, Abigail A Marsh, Johannes Schultz, René Hurlemann","doi":"10.1038/s41398-026-04302-0","DOIUrl":"10.1038/s41398-026-04302-0","url":null,"abstract":"<p><p>What makes some people willing to help strangers at a personal cost, while others are more hesitant or selective? Early life adversity - such as neglect or abuse - may shape how we respond to strangers in need later in life, yet the underlying neural mechanisms remain unclear. In this study we tested whether the neuropeptide oxytocin, a key modulator for a rich repertoire of social behaviours, influences altruistic decisions in adults with different childhood experiences. Using functional magnetic resonance imaging (fMRI) and a validated altruistic donation task, the study showed that oxytocin increased donations among individuals with greater childhood adversity, while reducing them in those with lower adversity. These behavioural effects were mirrored by changes in functional connectivity between the medial prefrontal cortex and middle cingulate cortex - core circuits involved in social evaluation and empathy. Our findings suggest that early life experiences sensitize neural pathways for social processing, and that oxytocin dynamically modulates these circuits to influence altruistic behaviour in adulthood.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13408452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148608008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coexistence of anhedonia and sensation-seeking with context-dependent gut dysbiosis in a prodromal transgenic mouse model of Parkinson's disease.","authors":"Olga Dubljević, Dušanka Popović, Milica Potrebić Stefanović, Branka Petković, Emilija Brdarić, Franziska Richter, Vesna Pešić","doi":"10.1038/s41398-026-04306-w","DOIUrl":"10.1038/s41398-026-04306-w","url":null,"abstract":"<p><p>Accumulating evidence indicates that gut microbiota plays a role in the progression of Parkinson's disease (PD). Microbiota-based treatments for prodromal PD, which is accompanied by a wide range of neuropsychiatric symptoms, are being considered a potential early intervention but are still under-investigated. This study examined the association between symptoms of affective and motivational impairments and gut dysbiosis in a transgenic mouse model (line G2-3) that overexpresses A53T mutant α-synuclein, a key protein involved in the disease pathology. By introducing biologically meaningful variations, such as genotype-based social grouping, efforts have been made to strengthen validity of the results and their translational relevance. Behavioral assessment was conducted on 6-month-old mice (the premotor stage) using Open Field, Elevated Plus Maze, Sucrose Preference and Tail Suspension tests. Fecal microbiota of mice was analyzed using 16S rRNA gene sequencing. Obtained data revealed a strong behavioral phenotype in transgenic mice expressed as co-occurrence of consummatory anhedonia and sensation-seeking/risk-taking behavior, without significant motivational deficits and with variable gut dysbiosis: mixed-genotype housing, among others, prominently favored Bacteroidaceae/Bacteroides, as observed in PD patients, while single-genotype housing increased Dubosiella, a key bacteria in gut-originated PD model, along with the enrichment of Bifidobacterium pseudolongum, a well-known health-promoting bacterium. Overall, using a mouse model with adequate construct validity, this study identifies challenges in novel strategies that consider gut microbiota as an early diagnostic and therapeutic target for PD; it highlights the potential of the examined transgenic strain in studying low hedonic tone- and sensation-seeking-associated PD prodrome, building the basis for personalized medicine.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149239625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From brain networks to peripheral signatures: candidate biomarkers for major depressive disorder.","authors":"Yuan Liu, Meijuan Li, Bo Yan, Ying Gao, Yifan Jing, Chengfeng Chen, Xue Tian, Yan Zhou, Mengxin Xie, Changlin Zhang, Bin Zhang, Jie Li","doi":"10.1038/s41398-026-04234-9","DOIUrl":"10.1038/s41398-026-04234-9","url":null,"abstract":"<p><p>Major depressive disorder (MDD) is a leading cause of disability worldwide, yet its neural basis and biomarkers remain elusive. In this study, we combined neuroimaging, transcriptomics, proteomics, and machine learning to bridge large-scale brain network dysfunction with peripheral molecular signatures. Resting-state functional magnetic resonance imaging (fMRI) from 544 MDD patients and 569 healthy controls (HC) revealed altered network topology involving thalamic, fronto-striatal, and parietal regions. Connectome-transcriptomic association analysis of these network alterations, in conjunction with differential gene expression analysis, identified 24 candidate genes, with FKBP5, PTX3, and APCDD1 prioritized by machine learning. Plasma proteomics further validated altered protein expression of the three prioritized genes in two independent cohorts (adults: 162 MDD patients and 103 HC; adolescents: 71 MDD patients and 39 HC). Protein-based diagnostic models achieved accuracies of 69.6% in adults and 83.1% in adolescents, while protein levels were significantly higher in adolescents with MDD than in HC (all P < 0.05). These findings suggest that PTX3, APCDD1, and FKBP5 may serve as candidate peripheral biomarkers associated with MDD-related brain network alterations.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13691126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149246470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autism with social anxiety is associated with acquiescent behaviors and enlarged amygdala volume.","authors":"Yu Hao, Sarah M Banker, Matthew Schafer, Ember Zhang, Sarah Barkley, Jadyn Trayvick, Arabella W Peters, Abigaël A Thinakaran, Christopher McLaughlin, Xiaosi Gu, Jennifer H Foss-Feig, Daniela Schiller","doi":"10.1038/s41398-026-04179-z","DOIUrl":"10.1038/s41398-026-04179-z","url":null,"abstract":"<p><p>Social anxiety (SA) frequently co-occurs with autism spectrum disorder (ASD), but it remains unclear whether SA in ASD reflects greater symptom severity or a distinct subtype. Across two complementary studies, we characterized the behavioral and neural correlates of SA in ASD using a naturalistic social navigation task measuring affiliative and power-related behaviors. In Study 1 (ASD = 575; controls = 357), autistic individuals with SA exhibited significantly reduced task-derived power behaviors (e.g., compliance with others' requests) compared to those without SA-a pattern not observed in non-autistic individuals. In Study 2 (ASD = 72; controls = 72), individuals with both ASD and SA showed enlarged amygdala volumes relative to both ASD without SA and non-autistic individuals. These behavioral and neural differences found in Study 1 and Study 2 were not observed in ASD with co-occurring depression or generalized anxiety disorder. Moreover, in Study 2, larger amygdala volume in the ASD group was associated with reduced task-derived power behaviors, indicating a neural signature linking social-behavioral differences and anxiety-related features. Together, these findings point to a distinct ASD phenotype marked by social anxiety, altered interpersonal dynamics, and amygdala enlargement, with implications for diagnosis and tailored intervention.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13686959/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149239650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lifestyle and BrainAGE in adult depression.","authors":"Nicole Sanford, Yuetong Yu, Ruiyang Ge, Shalaila S Haas, Liisa A M Galea, Sophia Frangou","doi":"10.1038/s41398-026-04297-8","DOIUrl":"10.1038/s41398-026-04297-8","url":null,"abstract":"<p><p>This study investigates how heterogeneity in lifestyle and physical fitness shapes patterns of brain ageing in depression. The study sample included medically healthy adults from the UK Biobank (44-82 years) with a history of depression (n = 896) and non-psychiatric controls (n = 36,206). Heterogeneity through Discriminative Analysis (HYDRA) was used to derive data-driven subgroups within the depression sample based on 224 behavioural and physical health features. Global and voxel-based brain-age-gap-estimates (brainAGE) computed from structural neuroimaging data were used for personalized assessment of brain ageing. Four depression clusters were identified: the \"balanced-active\" cluster (n = 253) characterized by an active lifestyle and balanced diet; the \"low metabolic risk-active\" cluster (n = 178) characterized by a health-conscious dietary and exercise lifestyle; the \"high metabolic risk-sedentary\" cluster (n = 315) who had higher body mass, poor diet, and sedentary behaviour; and the \"frailty-moderately active\" cluster (n = 150) who had a varied diet but coupled with physical frailty. Mood symptoms were lowest in the \"balanced-active\" cluster and highest in the \"high metabolic risk-sedentary\" cluster. While depression overall was associated with minimally accelerated global and local brain ageing in fronto-limbic regions, the \"high metabolic risk-sedentary\" cluster showed additional, regionally specific acceleration in prefrontal, parahippocampal, and thalamic areas. This work underscores the importance of lifestyle and fitness heterogeneity when examining associations between depression and neurobiological ageing and supports lifestyle-informed stratification as a pathway toward more targeted intervention strategies.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13687024/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149239672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coordinated response of vascular and glial cells in a pig model of sepsis.","authors":"Kimberly C Olney, J Hudson Barnett, Lauren E Tallant, Katelin Gibson, Kennedi Todd, Camila de Ávila, Piyush Hota, Adithya Shyamala Pandian, Pinar Cay Durgun, Michael Serhan, Ran Wang, Mary Laura Lind, Erica Forzani, Naomi M Gades, Leslie Thomas, John D Fryer","doi":"10.1038/s41398-026-04301-1","DOIUrl":"https://doi.org/10.1038/s41398-026-04301-1","url":null,"abstract":"<p><p>Sepsis is a deadly syndrome arising from overactivation of the immune system in response to a pathogen. Severe sepsis can result in sepsis-associated encephalopathy (SAE) that significantly contributes to morbidity and long-term cognitive impairment. Studying the molecular underpinnings of SAE in the human brain is challenging, and rodent models have limited translational applicability due to significant neuroanatomical and immune differences. To bridge this gap, we employed a Yorkshire pig model to investigate changes in the brain cortex during the early stages of SAE using a uropathogenic strain of E. coli to model bacterial sepsis. Bulk RNAseq of cortical brain demonstrated profound global shifts in immune and inflammatory pathways, cytokine signaling, vascular dysfunction, and homeostatic dysregulation. To gain a more granular understanding of the changes in this model, we performed single-nucleus RNA sequencing (snRNAseq) on the same cortical brain tissue. This snRNAseq analysis revealed dramatic alterations in vascular cell populations, accompanied by concomitant glial cell activation. Surprisingly minimal changes were noted in neurons, likely due to the very early nature of this insult. The neurovascular unit, including vascular leptomeningeal cells (VLMCs), mural cells, endothelial cells, astrocytes, and microglia, showed strong upregulation of genes involved in TNF signaling, cellular responses to cytokine stimuli, and cytokine signaling in the immune system. Conversely, downregulated genes were enriched in pathways related to the disruption of metabolic and structural functions, including genes involved in maintaining the blood-brain barrier (BBB). Cell-cell communication analysis also identified significant rewiring of intercellular signaling in the septic brain, with an overall increase in the number and strength of cell to cell interactions in the E. coli pigs compared to saline controls. In saline controls, cell-cell communication was dominated by homeostatic signaling from microglia and astrocytes. In contrast, the septic pigs showed a significant shift toward inflammatory and immune-related signaling pathways, mainly involving microglia and astrocytes, along with the emergence of signaling pathways from mural cells and VLMCs. Our findings reveal that systemic sepsis triggers a rapid shift from homeostatic to inflammatory signaling within the neurovascular unit, driven by the emergence of pro-inflammatory crosstalk between vascular cells, astrocytes, and microglia. This porcine model effectively captures the acute transcriptional landscape of the septic brain, offering a critical window for therapeutic strategies aimed at stabilizing the BBB and preventing long-term cognitive decline in sepsis survivors.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13633245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149115386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network localization of brain structural and functional alterations induced by electroconvulsive therapy for depression.","authors":"Shanwen Yao, Dao-Min Zhu, Huimin Zhu, Shuang Xu, Fan Mo, Jiajia Zhu, Yongqiang Yu","doi":"10.1038/s41398-026-04308-8","DOIUrl":"10.1038/s41398-026-04308-8","url":null,"abstract":"<p><p>Extensive longitudinal neuroimaging research has investigated brain structural and functional changes following electroconvulsive therapy (ECT) for depression. However, neither the regional nor the global brain effects reported in previous research can satisfactorily explain all aspects of the antidepressant efficacy of ECT, pointing to a potentially more refined network-specific mechanism. We initially identified the locations of brain structural and functional alterations induced by ECT for depression from 34 published studies, including 15 voxel-based morphometry studies with 596 depressed individuals and 19 resting-state functional magnetic resonance imaging studies with 436 depressed individuals. By combining these affected brain locations with large-scale brain functional connectome datasets (1113 healthy and 255 clinical individuals), we then adopted a novel functional connectivity network mapping approach to construct ECT-modulated structural and functional alteration networks. Our data showed different and specific ECT-modulated structural and functional alteration networks, with the former predominantly involving the subcortical (hippocampus and amygdala), ventral attention (insula and operculum and temporoparietal junction) and somatomotor (precentral and postcentral gyrus) networks, while the latter mainly implicating the default network (medial prefrontal cortex and posterior cingulate cortex). These findings may not only reconcile prior discrepancy between the ECT-induced regional and global brain changes from a network perspective, but also suggest a dissociation between the brain structural and functional effects of ECT.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"16 1","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13683337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149228483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}