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59,069 results on '"major depressive disorder"'

152. Disturbed sex hormone milieu in males and females with major depressive disorder and low-grade inflammation

Author

Lombardo, Giulia, Mondelli, Valeria, Worrell, Courtney, Sforzini, Luca, Mariani, Nicole, Nikkheslat, Naghmeh, Nettis, Maria A., Kose, Melisa, Zajkowska, Zuzanna, Cattaneo, Annamaria, Pointon, Linda, Turner, Lorinda, Cowen, Philip J., Drevets, Wayne C., Cavanagh, Jonathan, Harrison, Neil A., Bullmore, Edward T., Dazzan, Paola, and Pariante, Carmine M.

Published
2024
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174. Atlas of Gray Matter Volume Differences Across Psychiatric Conditions: A Systematic Review With a Novel Meta-Analysis That Considers Co-Occurring Disorders

Author

Fortea, Lydia, Ortuño, Maria, De Prisco, Michele, Oliva, Vincenzo, Albajes-Eizagirre, Anton, Fortea, Adriana, Madero, Santiago, Solanes, Aleix, Vilajosana, Enric, Yao, Yuanwei, Del Fabro, Lorenzo, Solé, Eduard, Verdolini, Norma, Farré-Colomés, Alvar, Serra-Blasco, Maria, Picó-Pérez, Maria, Lukito, Steve, Wise, Toby, Carlisi, Christina, Arnone, Danilo, Kempton, Matthew J., Hauson, Alexander Omar, Wollman, Scott, Soriano-Mas, Carles, Rubia, Katya, Norman, Luke, Fusar-Poli, Paolo, Mataix-Cols, David, Valentí, Marc, Via, Esther, Cardoner, Narcis, Solmi, Marco, Zhang, Jintao, Pan, Pinglei, Shin, Jae Il, Fullana, Miquel A., Vieta, Eduard, and Radua, Joaquim

Published
2024
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175. Machine learning models for diagnosis and risk prediction in eating disorders, depression, and alcohol use disorder

Author

Zhang, Zuo, Robinson, Lauren, Whelan, Robert, Jollans, Lee, Wang, Zijian, Nees, Frauke, Chu, Congying, Bobou, Marina, Du, Dongping, Cristea, Ilinca, Banaschewski, Tobias, Barker, Gareth J., Bokde, Arun L.W., Grigis, Antoine, Garavan, Hugh, Heinz, Andreas, Brühl, Rüdiger, Martinot, Jean-Luc, Martinot, Marie-Laure Paillère, Artiges, Eric, Orfanos, Dimitri Papadopoulos, Poustka, Luise, Hohmann, Sarah, Millenet, Sabina, Fröhner, Juliane H., Smolka, Michael N., Vaidya, Nilakshi, Walter, Henrik, Winterer, Jeanne, Broulidakis, M. John, van Noort, Betteke Maria, Stringaris, Argyris, Penttilä, Jani, Grimmer, Yvonne, Insensee, Corinna, Becker, Andreas, Zhang, Yuning, King, Sinead, Sinclair, Julia, Schumann, Gunter, Schmidt, Ulrike, and Desrivières, Sylvane

Published
2024
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193. Trajectory of peripheral inflammation during index ECT in association with clinical outcomes in treatment-resistant depression

Author

Hough, Christina M, Kruse, Jennifer L, Espinoza, Randall T, Brooks, John O, Congdon, Eliza J, Norris, Viviane, Craske, Michelle G, and Narr, Katherine L

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Major Depressive Disorder, Mental Illness, Mental Health, Depression, Serious Mental Illness, Brain Disorders, Mental health, Clinical sciences, Immunology
Abstract

Background: Electroconvulsive therapy (ECT) is a highly efficacious intervention for severe and intractable depression. Evidence suggests ECT provokes an initial acute inflammatory response that subsequently decreases with repeated administration. However, relationships between inflammatory changes and clinical effects are unclear. Improved understanding of these processes may provide critical insight into effective intervention for treatment-resistant depression (TRD). Methods: Plasma inflammatory markers were assessed at pre-treatment (T1), after the second ECT session (T2), and after ECT index series completion (post-treatment/T3) in TRD (n = 40). Changes were examined over time and in association with post-treatment Responder/Non-responder status (≥50% reduction in global depression severity) and percent change in affective, cognitive and neurovegetative depressive symptom domains. Results: C-reactive protein (CRP) and interleukin-6 (IL-6) increased from pre-treatment to T2, and decreased from T2 to post-treatment. Neither early (%T2-T1) nor total (%T1-T3) change in inflammation predicted clinical outcomes, however, the interaction between early/acute inflammatory response and post-treatment inflammation (relative to baseline) was associated with clinical outcomes. Larger initial increases in IL-6 predicted greater reductions in both affective and cognitive symptoms in subjects with higher post-treatment IL-6; those with lower post-treatment IL-6 trended toward the opposite. The same was found between changes in CRP and neurovegetative symptoms. Conclusions: Though preliminary, these results demonstrate how processes involved in the acute inflammatory response to ECT may differentially influence clinical outcomes depending on overall trajectory of inflammation following ECT. Findings also highlight the importance of examining symptom-specific changes in depression when studying treatment mechanisms, rather than relying solely on global measures of severity.

Published
2025

196. Comorbidity alters the genetic relationship between anxiety disorders and major depression

Author

Tesfaye, Markos, Shadrin, Alexey, Parker, Nadine, Jaholkowski, Piotr, Parekh, Pravesh, Kutrolli, Gleda, Birkenæs, Viktoria, Bakken, Nora R, Ask, Helga, Frei, Oleksandr, Djurovic, Srdjan, Dale, Anders M, Smeland, Olav B, O’Connell, Kevin S, and Andreassen, Ole A

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Behavioral and Social Science, Serious Mental Illness, Mental Health, Depression, Brain Disorders, Major Depressive Disorder, Human Genome, Anxiety Disorders, Mental Illness, 2.1 Biological and endogenous factors, 2.3 Psychological, social and economic factors, Mental health
Abstract

IMPORTANCE-: There is extensive comorbidity between anxiety disorders (ANX) and major depression (MD). Most studies on the genetics of ANX do not exclude comorbid cases of MD, and vice versa, therefore confounding genetic association analyses. Disorder-specific analysis of genomic data may reveal more precise biological pathways and causal relationships. OBJECTIVE-: To investigate the genetic relationship between disorder-specific ANX and MD compared to samples with comorbidity, including their causal relationship. DESIGN SETTING AND PARTICIPANTS-: Data from UK Biobank was used to perform genome-wide association studies (GWAS) of ANX-only and MD-only, and generate disorder-specific polygenic risk scores (PRS). The Norwegian Mother, Father, and Child Cohort (MoBa) was used to test the associations of PRS with diagnosis and symptoms. MD and ANX GWAS data including comorbidities (MD-co and ANX-co) were used as comparators. Genetic correlation was assessed using LDSC, and Mendelian randomization was employed to infer causal relationships. MAIN OUTCOMES AND MEASURES: GWAS of ICD-10 diagnoses of ANX, MD, or both. Genetic correlations between pairs of ANX and MD phenotypes. PRS associations with diagnoses of ANX, MD, and their comorbid states, and anxiety or depressive symptoms. RESULTS-: The GWAS of ANX-only (9,980 cases and 179,442 controls) and MD-only (15,301 cases and 179,038 controls) showed a lower genetic correlation (0.53) than the one between ANX-co and MD-co (0.90). ANX-only showed a causal relationship with MD-only (PFDR=1.5e-02), but not vice versa, while comorbid cases showed a significant bidirectional causal relationship (PFDR=2.9e-12, PFDR =9.3e-06). The PRS-MD-only were differentially associated with MD-only compared to ANX-only cases (β= -0.08; 95%CI: -0.11, -0.03); however, this differential association was not observed for the PRS-MD-co. A similar pattern of differential association with anxiety and depressive symptoms was observed for PRS-ANX-only, but not for PRS-MD-co. CONCLUSIONS AND RELEVANCE-: The genetics and underlying biology of ANX and MD are more distinct when comorbid cases are excluded from analyses and reveals that ANX may be causal for MD. This confounding of genetic relationships as a result of comorbidity is likely to apply to other psychiatric disorders. Disorder-specific genetic studies may help uncover more relevant biological mechanisms and guide more targeted clinical interventions.

Published
2024

197. Divergent patterns of genetic overlap between severe mental disorders and metabolic markers

Author

van der Meer, Dennis, Shadrin, Alexey A, Stinson, Sara E, Koch, Elise, Rokicki, Jaroslav, Rahman, Zillur, Bergstedt, Jacob, Ottas, Aigar, Sønderby, Ida E, Rødevand, Linn, Fuhrer, Julian, Quintana, Daniel S, Dale, Anders M, O’Connell, Kevin S, Djurovic, Srdjan, Lehto, Kelli, Alver, Maris, Milani, Lili, and Andreassen, Ole A

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Biological Psychology, Psychology, Schizophrenia, Obesity, Major Depressive Disorder, Diabetes, Behavioral and Social Science, Brain Disorders, Serious Mental Illness, Depression, Mental Illness, Mental Health, Cardiovascular, 2.1 Biological and endogenous factors, Metabolic and endocrine, Mental health, Good Health and Well Being
Abstract

Background Bipolar disorder (BIP), major depressive disorder (MDD) and schizophrenia (SCZ) are severe mental disorders (SMDs), each associated with poor cardiometabolic health. Mapping the genetic relationships of these highly heritable disorders with blood markers of metabolic activity may uncover biological pathways underlying this important shared clinical feature. Methods We charted global genetic overlap of the three SMDs, type 2 diabetes (T2D), coronary artery disease (CAD), and body mass index (BMI) with 249 circulating metabolic markers through linkage disequilibrium score regression and bivariate Gaussian mixture modeling. We estimated causal relationships, functionally annotated shared genetic variants, and investigated enrichment across diverse brain and body tissues. Results All three SMDs had extensive overlap with the metabolic markers. The pattern of genetic correlations was highly similar between MDD, T2D, CAD, and BMI (Spearmans correlation rs>.93), opposite in direction to the pattern found for SCZ and BIP (MDD-BIP rs=-.74; MDD-SCZ rs=-.83). The metabolic markers had widespread, robust causal effects on the SMDs and cardiometabolic traits. We mapped 1056 genes shared between the individual SMDs and the metabolic markers to disorder-specific processes related to metabolic activity, mitochondrial function, and synaptic processes. These genes were most prominently expressed throughout the brain, heart and liver. Discussion SMDs have strong associations with metabolic markers, whereby MDD has a distinctly different genetic relationship than BIP and SCZ. Our findings suggest that metabolic pathways are involved in the development of SMDs and can play a central role in disentangling disorder-specific etiologies. Our metabolic psychiatry approach has high potential to guide the development of targeted interventions.

Published
2024

198. A Comparative Study: Enhancing Conditional Generative Adversarial Networks for Functional Connectivity Synthesis in Major Depressive Disorder

Author

Oh, Ji-Hye, Jo, Eunjung, Kam, Tae-Eui, Goos, Gerhard, Series Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Yung, Moti, Editorial Board Member, Wallraven, Christian, editor, Liu, Cheng-Lin, editor, and Ross, Arun, editor

Published
2025
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199. Digital Mental Health Apps: Key Features and User Engagement for Better Wellness

Author

Rocha, Cristiana, Martinho, Diogo, Conceição, Luis, Novais, Paulo, Marreiros, Goreti, Goos, Gerhard, Series Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Yung, Moti, Editorial Board Member, Julian, Vicente, editor, Camacho, David, editor, Yin, Hujun, editor, Alberola, Juan M., editor, Nogueira, Vitor Beires, editor, Novais, Paulo, editor, and Tallón-Ballesteros, Antonio, editor

Published
2025
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200. A Literature Review on Predictive Classification of Major Depressive Disorder Using Advanced Data Analytics Techniques

Author

Mahender, Udutala, Arivalagan, S., Sathiyasuntharam, V., Sudhakar, P., Angrisani, Leopoldo, Series Editor, Arteaga, Marco, Series Editor, Chakraborty, Samarjit, Series Editor, Chen, Shanben, Series Editor, Chen, Tan Kay, Series Editor, Dillmann, Rüdiger, Series Editor, Duan, Haibin, Series Editor, Ferrari, Gianluigi, Series Editor, Ferre, Manuel, Series Editor, Jabbari, Faryar, Series Editor, Jia, Limin, Series Editor, Kacprzyk, Janusz, Series Editor, Khamis, Alaa, Series Editor, Kroeger, Torsten, Series Editor, Li, Yong, Series Editor, Liang, Qilian, Series Editor, Martín, Ferran, Series Editor, Ming, Tan Cher, Series Editor, Minker, Wolfgang, Series Editor, Misra, Pradeep, Series Editor, Mukhopadhyay, Subhas, Series Editor, Ning, Cun-Zheng, Series Editor, Nishida, Toyoaki, Series Editor, Oneto, Luca, Series Editor, Panigrahi, Bijaya Ketan, Series Editor, Pascucci, Federica, Series Editor, Qin, Yong, Series Editor, Seng, Gan Woon, Series Editor, Speidel, Joachim, Series Editor, Veiga, Germano, Series Editor, Wu, Haitao, Series Editor, Zamboni, Walter, Series Editor, Tan, Kay Chen, Series Editor, Kumar, Amit, editor, Gunjan, Vinit Kumar, editor, Senatore, Sabrina, editor, and Hu, Yu-Chen, editor

Published
2025
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