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Author reply to letter to the editor regarding "Efficacy and adverse effects of ketamine versus electroconvulsive therapy for major depressive disorder: A systematic review and meta-analysis."

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Journal of affective disorders 2024年 350卷 379-381页

作者： Luís Eduardo Gauer Stefanie Cavalcanti Debora de A Simoes Moreira Guilherme Teixeira João Quevedo Federal University of Paraná (UFPR) Curitiba PR Brazil. Translational Psychiatry Program Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth Houston) Houston TX USA Center of Excellence on Mood Disorders Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth Houston) Houston TX USA. Medical Sciences College of Santos Lusíada Foundation (UNILUS) Santos SP Brazil. University of Pernambuco (UPE) Recife PE Brazil. Center of Excellence on Mood Disorders Faillace Department of Psychiatry and Behavioral Sciences McGovern Medical School The University of Texas Health Science Center at Houston (UTHealth Houston) Houston TX USA Neuroscience Graduate Program The University of Texas MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences Houston TX USA Translational Psychiatry Laboratory Graduate Program in Health Sciences University of Southern Santa Catarina (UNESC) Criciúma SC Brazil. Electronic address: joao.l.dequevedo@uth.tmc.edu.

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SAT0588 Early Cerebral Volume Reduction and Regional Improvement of Prefrontal Gray Matter Volume with Reduced Lupus Disease Activity in Patients with Newly-Diagnosed Non-Neuropsychiatric Systemic Lupus Erythematosus (SLE)

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Annals of the Rheumatic Diseases 2015年 74卷 874-874页

作者： A. Mak R.C. Ho H.Y. Tng H.L. Koh J.S. Chong J.H. Zhou 1Medicine 2Psychological Medicine National University of Singapore 3Center for Cognitive Neuroscience Neuroscience and Behavioral Disorders Program Duke-National University of Singapore Graduate Medical School Singapore Singapore

Background Cerebral volume loss is evident in patients within 9 months of the diagnosis of SLE. As potentially neurotoxic autoantibodies can be present many years before SLE symptoms emerge, cerebral volume loss would theoretically commence even much earlier before the clinical onset of SLE. Also, while it has been suggested that SLE-related inflammation negatively impacts on brain volume, whether reducing SLE disease activity can improve cerebral volume in SLE patients is unknown. Objectives We evaluated if the volumes of the gray matter (GMV) and white matter (WMV) of the brains of newly-diagnosed SLE patients would be reduced as compared to those of age-, sex- and IQ-matched healthy controls (HC). We also investigated for potential regional improvement of GMV and WMV after SLE patients achieved low disease activity (SLEDAI<4). If so, we would further address if reducing disease activity early in the course of SLE would correlate with enhanced cerebral volumes in SLE patients. Methods T1-weighted MRI brain images acquired by a 1.5T Siemens Symphony MRI scanner were obtained from 14 HC and 14 SLE patients within 5 months of their diagnosis (S1) and after attaining low disease activity (S2) with ≥6 months of immunosuppressive therapy. Whole brain voxel-based morphometry was used to detect differences in the GMV and WMV between SLE patients and HC and those between the SLE group at S1 and S2. To examine GMV and WMV changes within the SLE group between S1 and S2, whole brain voxelwise paired t-tests between subject-level GMV (and WMV) probabilistic maps in SLE patients at S1 and S2 was performed at p<0.001 with a minimum cluster size of 980 voxels. Patients with neuropsychiatric symptoms, traditional cardiovascular risk factors, anti-cardiolipin antibodies and lupus anticoagulant were excluded as these factors may engender cerebral volume loss independent of SLE. Results The mean ± SD age of the SLE patients and HC was 39.38±13.9 and 34.07±14.4 years respectively, wit

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乌头碱诱发心律失常毒性新分子机制#

乌头碱诱发心律失常毒性新分子机制#

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第四届（2023年）中国安全药理学学术年会

作者：王相冲 Jianjun Wu Heming Wei 许彦芳苏素文河北医科大学药理教研室 Neuroscience & Behavioral Disorders Program Duke-NUS Medical School Singapore Research Laboratory KK Women's & Children's HospitalSingapore

目的:乌头类中药被誉为"回阳救逆"第一要药,其应用历史悠久、临床疗效显著。然而,其主要活性成分乌头碱有明显的毒性,主要表现为中枢神经系统和心血管系统的毒性反应,特别是其心脏毒性,可引起致死性心律失常,严重危害人类健... 详细信息

目的:乌头类中药被誉为"回阳救逆"第一要药,其应用历史悠久、临床疗效显著。然而,其主要活性成分乌头碱有明显的毒性,主要表现为中枢神经系统和心血管系统的毒性反应,特别是其心脏毒性,可引起致死性心律失常,严重危害人类健康。然而,乌头碱致心律失常的机制尚不明确。因此,本研究采用整体动物实验和体外细胞实验相结合的方法,对乌头碱致心律失常的分子细胞学机制进行探讨。

关键词：心律失常浓度依赖性心室肌细胞乌头碱钙电流钠电流动作电位时程分子机制

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Treatment response biomarkers in anxiety disorders: From neuroimaging to neuronally-derived extracellular vesicles and beyond

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Biomarkers in Neuropsychiatry 2020年 3卷 100024-100024页

作者： Strawn, Jeffrey R. Levine, Amir Department of Psychiatry and Behavioral Neuroscience Anxiety Disorders Research Program College of Medicine University of Cincinnati Cincinnati OH United States Department of Pediatrics Division of Child & Adolescent Psychiatry and Division of Clinical Pharmacology Cincinnati Children's Hospital Medical Center Cincinnati OH United States Department of Psychiatry Columbia University and New York State Psychiatric Institute New York NY United States

Multiple and diverse psychotherapeutic or psychopharmacologic treatments effectively reduce symptoms for many patients with anxiety disorders, but the trajectory and magnitude of response vary considerably. This heterogeneity of treatment response has invigorated the search for biomarkers of treatment response in anxiety disorders, across the lifespan. In this review, we summarize evidence for biomarkers of treatment response in children, adolescents and adults with generalized, separation and social anxiety disorders as well as panic disorder. We then discuss the relationship between these biomarkers of treatment response and the pathophysiology of anxiety disorders. Finally, we provide context for treatment response biomarkers of the future, including neuronally-derived extracellular vesicles in anxiety disorders and discuss challenges that must be overcome prior to the debut of treatment response biomarkers in the clinic. A number of promising treatment response biomarkers have been identified, although there is an urgent need to replicate findings and to identify which biomarkers might guide clinicians in selecting from available treatments rather than just simply identifying patients who may be less likely to respond to a given intervention. © 2020 The Author(s)

关键词： fMRI Generalized anxiety disorder Pharmacogenomics Separation anxiety disorder

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Pediatric anxiety and daily fine particulate matter: A longitudinal study

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Psychiatry Research Communications 2022年第4期2卷 100077页

作者： Vancil, Andrew Strawn, Jeffrey R. Rasnick, Erika Levine, Amir Schroeder, Heidi K. Specht, Ashley M. Turner, Ashley L. Ryan, Patrick H. Brokamp, Cole Cincinnati Children's Hospital Medical Center Division of Biostatistics and Epidemiology United States University of Cincinnati Anxiety Disorders Research Program Department of Psychiatry & Behavioral Neuroscience United States Department of Psychiatry College of Physicians and Surgeons Columbia University United States Division of Child and Adolescent Psychiatry New York State Psychiatric Institute United States University of Cincinnati College of Medicine Department of Pediatrics United States

Daily variations in ambient fine particulate matter (PM2.5) could contribute to the morbidity of anxiety disorders in children and adolescents, but has not yet been studied longitudinally at a daily level. We tested t...

Daily variations in ambient fine particulate matter (PM_2.5) could contribute to the morbidity of anxiety disorders in children and adolescents, but has not yet been studied longitudinally at a daily level. We tested this association using repeated weekly measures of anxiety symptom severity in a group of 23 adolescents with generalized anxiety disorder. After estimating ambient PM_2.5 concentrations using a validated model, we found that increased concentrations were significantly associated with increased anxiety symptom severity and frequency two, three, and four days later. PM_2.5 may be a novel, modifiable exposure that could inform population level interventions to decrease psychiatric morbidity. © 2022 The Authors

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Focal Clusters of Peri-Synaptic Matrix Contribute to Activity-Dependent Plasticity and Memory

SSRN

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SSRN 2023年

作者： Chelini, Gabriele Mirzapourdelavar, Hadi Durning, Peter Baidoe-Ansah, David O’Donovan, Sinead M. Klengel, Torsten Balasco, Luigi Berciu, Cristina Boyer-Boiteau, Anne Smith, Robert Ressler, Kerry J. Bozzi, Yuri Dityatev, Alexander Berretta, Sabina Translational Neuroscience Laboratory McLean Hospital BelmontMA United States Department of Psychiatry Harvard Medical School BostonMA United States DZNE Molecular Neuroplasticity Magdeburg Germany Cognitive Disorders Research Laboratory University of Toledo ToledoOH United States Translational Molecular Genomics Laboratory Mclean Hospital BelmontMA United States University Medical Center Göttingen Department of Psychiatry Göttingen Germany Center for Mind/Brain Science University of Trento Rovereto Italy Program in Neuroscience Harvard Medical School BostonMA United States Neurobiology of Fear Laboratory McLean Hospital BelmontMA United States CNR Neuroscience Institute Pisa Italy Medical Faculty Otto von Guericke University Magdeburg Germany Center for Behavioral Brain Sciences Otto von Guericke University Magdeburg Germany

Experience-dependent learning depends on synaptic plasticity. Recent findings show that effective integration of novel salient information requires coordinated processes of homo- and hetero- synaptic plasticity onto neighboring dendritic stretches. In this work, we hypothesized that activity-dependent remodeling of the peri-synaptic extracellular matrix contributes to this mechanism. We show that clusters of the peri-synaptic matrix, containing the 6-sulfated chondroitin sulfate proteoglycan versican ( Vcan-CSPG ), emerge in response to sensory stimuli, showing temporal and spatial coincidence with the dendritic spine plasticity. Moreover, the depletion of Vcan-CSPG in the CA1 hippocampal region was accompanied by impaired long-term potentiation and object location memory in adult mice. These findings show that a specific CSPG glycoform regulates the molecular mechanisms underlying induction and consolidation of synaptic plasticity, confirming that experience-dependent refinement of the brain extracellular matrix plays a critical role in learning and memory. © 2023, The Authors. All rights reserved.

关键词： Sulfur compounds

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Consensus guidelines for assessing eligibility of pathogenic DNA variants for antisense oligonucleotide treatments

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American Journal of Human Genetics 2025年第5期112卷 975-983页

作者： Cheerie, David Meserve, Margaret M. Beijer, Danique Kaiwar, Charu Newton, Logan Taylor Tavares, Ana Lisa Verran, Aubrie Soucy Sherrill, Emma Leonard, Stefanie Sanders, Stephan J. Blake, Emily Elkhateeb, Nour Gandhi, Aastha Liang, Nicole S.Y. Morgan, Jack T. Verwillow, Anna Verheijen, Jan Giles, Andrew Williams, Sean Chopra, Maya Croft, Laura Dafsari, Hormos Salimi Davidson, Alice E. Friedman, Jennifer Gregor, Anne Haque, Bushra Lechner, Rosan Montgomery, Kylie-Ann Ryten, Mina Schober, Emil Siegel, Gabriele Sullivan, Patricia J. Whittle, Ella F. Zardetto, Bianca Yu, Timothy W. Synofzik, Matthis Aartsma-Rus, Annemieke Costain, Gregory Lauffer, Marlen C. Program in Genetics & Genome Biology SickKids Research Institute Toronto M5G 0A4 ON Canada Department of Molecular Genetics University of Toronto Toronto M5S 1A8 ON Canada Division of Genetics and Genomics Boston Children's Hospital Boston 02115 MA United States Division of Translational Genomics of Neurodegenerative Diseases Hertie Institute for Clinical Brain Research and Center of Neurology University of Tübingen Tübingen 72076 Germany German Center of Neurodegenerative Diseases (DZNE) Tübingen 72076 Germany Clinical Molecular Geneticist Department of Pathology and Laboratory Medicine Precision Diagnostics Laboratory Children's Hospital Colorado Aurora 80045 CO United States Genomics England London E14 5AB United Kingdom Department of Clinical Genetics Cambridge University Hospitals NHS Foundation Trust Cambridge Cambridgeshire CB2 0QQ United Kingdom N=1 Collaborative 7 Carole Place Somerville 02143 MA United States Institute of Developmental and Regenerative Medicine Department of Pediatrics University of Oxford Oxford OX3 7TY United Kingdom Department of Psychiatry and Behavioral Sciences UCSF Weill Institute for Neurosciences University of California San Francisco San Francisco 94158 CA United States New York Genome Center New York 10013 NY United States Department of Quantitative Health Sciences Mayo Clinic Rochester 55902 MN United States Division of Clinical & Metabolic Genetics Hospital for Sick Children Toronto M5G 1X8 ON Canada Department of Genetic Counselling Hospital for Sick Children Toronto M5G 1X8 ON Canada Dutch Center for RNA Therapeutics Department of Human Genetics Leiden University Medical Center Leiden 2333 ZA Netherlands Center for Genomic Medicine Massachusetts General Hospital 55 Fruit Street Boston 02114 MA United States Department of Pathology University of Utah School of Medicine Salt Lake City 84112 UT United States ARUP Laboratories Salt Lake City 84108 UT United States Ambry Genetics 1 E

Of the around 7,000 known rare diseases worldwide, disease-modifying treatments are available for fewer than 5%, leaving millions of individuals without specialized therapeutic strategies. In recent years, antisense oligonucleotides (ASOs) have shown promise as individualized genetic interventions for rare genetic diseases. However, there is currently no consensus on which disease-causing DNA variants are suitable candidates for this type of genetic therapy. The patient identification working group of the N=1 Collaborative (N1C), alongside an international group of volunteer assessors, has developed and piloted consensus guidelines for assessing the eligibility of pathogenic DNA variants for ASO treatments. We herein present the N1C VARIANT (variant assessments toward eligibility for antisense oligonucleotide treatment) guidelines, including the guiding scientific principles and our approach to consensus building. Pathogenic, disease-causing variants can be assessed for the three currently best-established ASO treatment approaches: splice correction, exon skipping, and downregulation of RNA transcripts. A genetic variant is classified as “eligible,” “likely eligible,” “unlikely eligible,” or “not eligible” in relation to the different approaches or as “unable to assess.” We also review key considerations related to assessing the upregulation of transcripts from the wild-type allele, an emerging ASO therapeutic strategy. We provide additional tools and training materials to enable clinicians and researchers to use these guidelines for their eligibility assessments. With this initial edition of our N1C VARIANT guidelines, we provide the rare genetic disease community with guidance on how to identify suitable candidates for variant-specific ASO-based therapies and the possibility of integrating such assessments into routine clinical practice. © 2025 The Authors

关键词： antisense oligonucleotides consensus guidelines individualized genetic therapies personalized medicine rare genetic diseases

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Features associated with diet pill use in individuals with eating disorders

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Eating Behaviors 2008年第1期9卷 73-81页

作者： Reba-Harrelson, Lauren Von Holle, Ann Thornton, Laura M. Klump, Kelly L. Berrettini, Wade H. Brandt, Harry Crawford, Steven Crow, Scott Fichter, Manfred M. Goldman, David Halmi, Katherine A. Johnson, Craig Kaplan, Allan S. Keel, Pamela LaVia, Maria Mitchell, James Plotnicov, Katherine Rotondo, Alessandro Strober, Michael Treasure, Janet Woodside, D. Blake Kaye, Walter H. Bulik, Cynthia M. Department of Psychiatry University of North Carolina at Chapel Hill NC United States Department of Psychiatry University of Pittsburgh Medical Center Western Psychiatric Institute and Clinic Pittsburgh PA United States Department of Psychology Michigan State University East Lansing MI United States Center of Neurobiology and Behavior University of Pennsylvania Philadelphia PA United States Center for Eating Disorders Sheppard Pratt Health System Towson MD United States Department of Psychiatry University of Minnesota Minneapolis MN United States Klinik Roseneck Hospital for Behavioral Medicine University of Munich (LMU) Germany National Institute of Alcohol Abuse and Alcoholism Rockville MD United States Weill Cornell Medical College New York Presbyterian Hospital - Westchester Division White Plains NY United States Laureate Psychiatric Clinic and Hospital Tulsa OK United States Program for Eating Disorders Toronto General Hospital University Health Network Canada Department of Psychology University of Iowa United States University of North Dakota School of Medicine and Health Sciences Department of Clinical Neuroscience Neuropsychiatric Research Institute Fargo ND United States Department of Psychiatry Pharmacology and Biotechnologies University of Pisa Pisa Italy UCLA Semel Institute for Neuroscience and Human Behavior David Geffen School of Medicine University of California at Los Angeles Los Angeles CA United States Department of Psychiatry Institute of Psychiatry King's College London England United Kingdom Department of Psychiatry University of Toronto Toronto Canada Department of Nutrition University of North Carolina Chapel Hill NC United States

We investigated the relation between diet pill use and eating disorder subtype, purging and other compensatory behaviors, body mass index (BMI), tobacco and caffeine use, alcohol abuse or dependence, personality characteristics, and Axis I and Axis II disorders in 1,345 participants from the multisite Price Foundation Genetics Studies. Diet pill use was significantly less common in women with restricting type of AN than in women with other eating disorder subtypes. In addition, diet pill use was associated with the use of multiple weight control behaviors, higher BMI, higher novelty seeking, and the presence of anxiety disorders, alcohol abuse or dependence, and borderline personality disorder. Findings suggest that certain clinical and personality variables distinguish individuals with eating disorders who use diet pills from those who do not. In the eating disorder population, vigilant screening for diet pill use should be routine clinical practice. © 2007 Elsevier Ltd. All rights reserved.

关键词： Diet pills Eating disorders Novelty seeking Weight control behaviors

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Correction: Progressive decline in hippocampal CA1 volume in individuals at ultra-high-risk for psychosis who do not remit: findings from the longitudinal youth at risk study

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Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 2019年第12期44卷 2144页

作者： New Fei Ho Daphne J Holt Mike Cheung Juan Eugenio Iglesias Alex Goh Mingyuan Wang Joseph K W Lim Joshua de Souza Joann S Poh Yuen Mei See R Alison Adcock Stephen J Wood Michael W L Chee Jimmy Lee Juan Zhou Institute of Mental Health Singapore Singapore. new_fei_ho@imh.com.sg. Neuroscience and Behavioral Disorders Program Center for Cognitive Neuroscience Duke-National University of Singapore Graduate Medical School Singapore Singapore. new_fei_ho@imh.com.sg. Department of Psychiatry Massachusetts General Hospital and Harvard Medical School Boston MA USA. Department of Psychology National University of Singapore Singapore Singapore. University College London London UK. Institute of Mental Health Singapore Singapore. Neuroscience and Behavioral Disorders Program Center for Cognitive Neuroscience Duke-National University of Singapore Graduate Medical School Singapore Singapore. Center for Cognitive Neuroscience Duke University Durham NC USA. School of Psychology University of Birmingham Birmingham UK. Neuroscience and Behavioral Disorders Program Center for Cognitive Neuroscience Duke-National University of Singapore Graduate Medical School Singapore Singapore. helen.zhou@duke-nus.edu.sg.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Genome-wide analyses identify 30 loci associated with obsessive–compulsive disorder

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Nature Genetics 2025年 1-13页

作者： Strom, Nora I. Gerring, Zachary F. Galimberti, Marco Yu, Dongmei Halvorsen, Matthew W. Abdellaoui, Abdel Rodriguez-Fontenla, Cristina Sealock, Julia M. Bigdeli, Tim Coleman, Jonathan R. Mahjani, Behrang Thorp, Jackson G. Bey, Katharina Burton, Christie L. Luykx, Jurjen J. Zai, Gwyneth Alemany, Silvia Andre, Christine Askland, Kathleen D. Bäckman, Julia Banaj, Nerisa Barlassina, Cristina Nissen, Judith Becker Bienvenu, O. Joseph Black, Donald Bloch, Michael H. Børte, Sigrid Bosch, Rosa Breen, Michael Brennan, Brian P. Brentani, Helena Buxbaum, Joseph D. Bybjerg-Grauholm, Jonas Byrne, Enda M. Cabana-Dominguez, Judit Camarena, Beatriz Camarena, Adrian Cappi, Carolina Carracedo, Angel Casas, Miguel Cavallini, Maria Cristina Ciullo, Valentina Cook, Edwin H. Crosby, Jesse Cullen, Bernadette A. De Schipper, Elles J. Delorme, Richard Djurovic, Srdjan Elias, Jason A. Estivill, Xavier Falkenstein, Martha J. Fundin, Bengt T. Garner, Lauryn Gironda, Christina Goes, Fernando S. Grados, Marco A. Grove, Jakob Guo, Wei Haavik, Jan Hagen, Kristen Harrington, Kelly Havdahl, Alexandra Höffler, Kira D. Hounie, Ana G. Hucks, Donald Hultman, Christina Janecka, Magdalena Jenike, Eric Karlsson, Elinor K. Kelley, Kara Klawohn, Julia Krasnow, Janice E. Krebs, Kristi Lange, Christoph Lanzagorta, Nuria Levey, Daniel Lindblad-Toh, Kerstin Macciardi, Fabio Maher, Brion Mathes, Brittany McArthur, Evonne McGregor, Nathaniel McLaughlin, Nicole C. Meier, Sandra Miguel, Euripedes C. Mulhern, Maureen Nestadt, Paul S. Nurmi, Erika L. O’Connell, Kevin S. Osiecki, Lisa Ousdal, Olga Therese Palviainen, Teemu Pedersen, Nancy L. Piras, Federica Potluri, Sriramya Rabionet, Raquel Ramirez, Alfredo Rauch, Scott Reichenberg, Abraham Riddle, Mark A. Ripke, Stephan Rosário, Maria C. Sampaio, Aline S. Schiele, Miriam A. Skogholt, Anne Heidi Sloofman, Laura G. Smit, Jan Artigas, María Soler Thomas, Laurent F. Tifft, Eric Vallada, Homero van Kirk, Nathanial Veenstra-VanderWeele, Jeremy Vulink, Nienke N. Walker, Christopher P. Wang, Ying Wendland, Jens R. Winsvold Department of Psychology Humboldt-Universität zu Berlin Berlin Germany Department of Psychiatric Phenomics and Genomics (IPPG) Ludwig-Maximilians University Munich Munich Germany Centre for Psychiatry Research Department of Clinical Neuroscience Karolinska Institutet and Stockholm Health Services Region Stockholm Stockholm Sweden Department of Biomedicine Aarhus University Aarhus Denmark University Hospital of Psychiatry and Psychotherapy University of Bern Bern Switzerland Department of Mental Health and Neuroscience Translational Neurogenomics QIMR Berghofer Medical Research Institute Brisbane QLD Australia Department of Population Health and Immunity Healthy Development and Ageing Walter and Eliza Hall Institute of Medical Research Melbourne VIC Australia Department of Psychiatry Human Genetics Yale University New Haven CT United States VA Connecticut Healthcare System West Haven CT United States Department of Center for Genomic Medicine Psychiatric and Neurodevelopmental Genetics Unit Massachusetts General Hospital Boston MA United States Stanley Center for Psychiatric Research Broad Institute of MIT and Harvard Cambridge MA United States Department of Genetics University of North Carolina at Chapel Hill Chapel Hill NC United States Department of Psychiatry Amsterdam University Medical Centers University of Amsterdam Amsterdam Netherlands Center for Research in Molecular Medicine and Chronic Diseases (CiMUS) Genomics and Bioinformatics University of Santiago de Compostela Santiago de Compostela Spain Grupo de Medicina Xenómica Genetics Instituto de Investigación Sanitaria de Santiago de Compostela (FIDIS) Santiago de Compostela Spain Vanderbilt Genetics Institute Vanderbilt University Nashville TN United States Department of Psychiatry and Behavioral Sciences SUNY Downstate Health Sciences University Brooklyn NY United States VA NY Harbor Healthcare System Brooklyn NY United States Social Genetic and Developmental Psychiatry Centre Insti

Obsessive–compulsive disorder (OCD) affects ~1% of children and adults and is partly caused by genetic factors. We conducted a genome-wide association study (GWAS) meta-analysis combining 53,660 OCD cases and 2,044,417 controls and identified 30 independent genome-wide significant loci. Gene-based approaches identified 249 potential effector genes for OCD, with 25 of these classified as the most likely causal candidates, including WDR6, DALRD3 and CTNND1 and multiple genes in the major histocompatibility complex (MHC) region. We estimated that ~11,500 genetic variants explained 90% of OCD genetic heritability. OCD genetic risk was associated with excitatory neurons in the hippocampus and the cortex, along with D₁ and D₂ type dopamine receptor-containing medium spiny neurons. OCD genetic risk was shared with 65 of 112 additional phenotypes, including all the psychiatric disorders we examined. In particular, OCD shared genetic risk with anxiety, depression, anorexia nervosa and Tourette syndrome and was negatively associated with inflammatory bowel diseases, educational attainment and body mass index. © The Author(s) 2025.

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