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1. Single cell sequencing of radial glia progeny reveals the diversity of newborn neurons in the adult zebrafish brain.

Author

Lange C, Rost F, Machate A, Reinhardt S, Lesche M, Weber A, Kuscha V, Dahl A, Rulands S, and Brand M

Subjects
Animals, Animals, Genetically Modified, Animals, Newborn anatomy & histology, Diencephalon cytology, Gene Expression Profiling, Mice, Sequence Analysis, RNA, Single-Cell Analysis, Telencephalon cytology, Zebrafish growth & development, Brain cytology, Cell Lineage, Ependymoglial Cells cytology, Neurogenesis, Neurons cytology, Zebrafish anatomy & histology
Abstract

Zebrafish display widespread and pronounced adult neurogenesis, which is fundamental for their regeneration capability after central nervous system injury. However, the cellular identity and the biological properties of adult newborn neurons are elusive for most brain areas. Here, we have used short-term lineage tracing of radial glia progeny to prospectively isolate newborn neurons from the her4.1 + radial glia lineage in the homeostatic adult forebrain. Transcriptome analysis of radial glia, newborn neurons and mature neurons using single cell sequencing identified distinct transcriptional profiles, including novel markers for each population. Specifically, we detected two separate newborn neuron types, which showed diversity of cell fate commitment and location. Further analyses showed that these cell types are homologous to neurogenic cells in the mammalian brain, identified neurogenic commitment in proliferating radial glia and indicated that glutamatergic projection neurons are generated in the adult zebrafish telencephalon. Thus, we prospectively isolated adult newborn neurons from the adult zebrafish forebrain, identified markers for newborn and mature neurons in the adult brain, and revealed intrinsic heterogeneity among adult newborn neurons and their homology with mammalian adult neurogenic cell types., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)

Published
2020
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2. Sequence and expression levels of circular RNAs in progenitor cell types during mouse corticogenesis.

Author

Dori M, Haj Abdullah Alieh L, Cavalli D, Massalini S, Lesche M, Dahl A, and Calegari F

Subjects
Alternative Splicing genetics, Animals, Binding Sites, Cerebellar Cortex cytology, Exons genetics, Female, Mice, Mice, Transgenic, MicroRNAs genetics, MicroRNAs metabolism, Pregnancy, Protein Biosynthesis genetics, RNA, Circular metabolism, RNA, Messenger genetics, Base Sequence genetics, Neurogenesis genetics, RNA, Circular genetics, Stem Cells physiology, Transcriptome genetics
Abstract

Circular (circ) RNAs have recently emerged as a novel class of transcripts whose identification and function remain elusive. Among many tissues and species, the mammalian brain is the organ in which circRNAs are more abundant and first evidence of their functional significance started to emerge. Yet, even within this well-studied organ, annotation of circRNAs remains fragmentary, their sequence is unknown, and their expression in specific cell types was never investigated. Overcoming these limitations, here we provide the first comprehensive identification of circRNAs and assessment of their expression patterns in proliferating neural stem cells, neurogenic progenitors, and newborn neurons of the developing mouse cortex. Extending the current knowledge about the diversity of this class of transcripts by the identification of nearly 4,000 new circRNAs, our study is the first to provide the full sequence information and expression patterns of circRNAs in cell types representing the lineage of neurogenic commitment. We further exploited our data by evaluating the coding potential, evolutionary conservation, and biogenesis of circRNAs that we found to arise from a specific subclass of linear mRNAs. Our study provides the arising field of circRNA biology with a powerful new resource to address the complexity and potential biological significance of this new class of transcripts., (© 2019 Dori et al.)

Published
2019
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3. 3D Culture Method for Alzheimer's Disease Modeling Reveals Interleukin-4 Rescues Aβ42-Induced Loss of Human Neural Stem Cell Plasticity.

Author

Papadimitriou C, Celikkaya H, Cosacak MI, Mashkaryan V, Bray L, Bhattarai P, Brandt K, Hollak H, Chen X, He S, Antos CL, Lin W, Thomas AK, Dahl A, Kurth T, Friedrichs J, Zhang Y, Freudenberg U, Werner C, and Kizil C

Subjects
Adult, Aged, 80 and over, Alzheimer Disease, Animals, Brain metabolism, Cell Proliferation physiology, Cells, Cultured, Disease Models, Animal, Female, Humans, Kynurenic Acid metabolism, Male, Mice, Mice, Transgenic, Middle Aged, Neural Stem Cells physiology, Neurons cytology, Transaminases metabolism, Transcriptional Activation genetics, Young Adult, Amyloid beta-Peptides metabolism, Cell Plasticity physiology, Interleukin-4 metabolism, Neural Stem Cells cytology, Neurogenesis physiology
Abstract

Neural stem cells (NSCs) constitute an endogenous reservoir for neurons that could potentially be harnessed for regenerative therapies in disease contexts such as neurodegeneration. However, in Alzheimer's disease (AD), NSCs lose plasticity and thus possible regenerative capacity. We investigate how NSCs lose their plasticity in AD by using starPEG-heparin-based hydrogels to establish a reductionist 3D cell-instructive neuro-microenvironment that promotes the proliferative and neurogenic ability of primary and induced human NSCs. We find that administration of AD-associated Amyloid-β42 causes classical neuropathology and hampers NSC plasticity by inducing kynurenic acid (KYNA) production. Interleukin-4 restores NSC proliferative and neurogenic ability by suppressing the KYNA-producing enzyme Kynurenine aminotransferase (KAT2), which is upregulated in APP/PS1dE9 mouse model of AD and in postmortem human AD brains. Thus, our culture system enables a reductionist investigation of regulation of human NSC plasticity for the identification of potential therapeutic targets for intervention in AD., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Published
2018
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4. IL4/STAT6 Signaling Activates Neural Stem Cell Proliferation and Neurogenesis upon Amyloid-β42 Aggregation in Adult Zebrafish Brain.

Author

Bhattarai P, Thomas AK, Cosacak MI, Papadimitriou C, Mashkaryan V, Froc C, Reinhardt S, Kurth T, Dahl A, Zhang Y, and Kizil C

Subjects
Aging pathology, Animals, Brain pathology, Cell Plasticity, Cell Proliferation, Microglia, Nerve Degeneration pathology, Neural Stem Cells cytology, Neurons, Phenotype, Zebrafish metabolism, Amyloid beta-Peptides metabolism, Brain metabolism, Interleukin-4 metabolism, Neurogenesis, Peptide Fragments metabolism, Protein Aggregates, STAT6 Transcription Factor metabolism, Signal Transduction
Abstract

Human brains are prone to neurodegeneration, given that endogenous neural stem/progenitor cells (NSPCs) fail to support neurogenesis. To investigate the molecular programs potentially mediating neurodegeneration-induced NSPC plasticity in regenerating organisms, we generated an Amyloid-β42 (Aβ42)-dependent neurotoxic model in adult zebrafish brain through cerebroventricular microinjection of cell-penetrating Aβ42 derivatives. Aβ42 deposits in neurons and causes phenotypes reminiscent of amyloid pathophysiology: apoptosis, microglial activation, synaptic degeneration, and learning deficits. Aβ42 also induces NSPC proliferation and enhanced neurogenesis. Interleukin-4 (IL4) is activated primarily in neurons and microglia/macrophages in response to Aβ42 and is sufficient to increase NSPC proliferation and neurogenesis via STAT6 phosphorylation through the IL4 receptor in NSPCs. Our results reveal a crosstalk between neurons and immune cells mediated by IL4/STAT6 signaling, which induces NSPC plasticity in zebrafish brains., (Copyright © 2016 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2016
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5. Human-specific gene ARHGAP11B promotes basal progenitor amplification and neocortex expansion.

Author

Florio M, Albert M, Taverna E, Namba T, Brandl H, Lewitus E, Haffner C, Sykes A, Wong FK, Peters J, Guhr E, Klemroth S, Prüfer K, Kelso J, Naumann R, Nüsslein I, Dahl A, Lachmann R, Pääbo S, and Huttner WB

Subjects
Animals, Cell Separation, GTPase-Activating Proteins chemistry, GTPase-Activating Proteins genetics, Gene Duplication, Humans, Lateral Ventricles cytology, Mice, Neocortex cytology, Neocortex metabolism, Neural Stem Cells metabolism, Neuroglia cytology, Neuroglia metabolism, Neurons cytology, Neurons metabolism, Protein Structure, Tertiary, Transcriptome, GTPase-Activating Proteins physiology, Gene Expression Regulation, Developmental, Neocortex embryology, Neural Stem Cells cytology, Neurogenesis genetics
Abstract

Evolutionary expansion of the human neocortex reflects increased amplification of basal progenitors in the subventricular zone, producing more neurons during fetal corticogenesis. In this work, we analyze the transcriptomes of distinct progenitor subpopulations isolated by a cell polarity-based approach from developing mouse and human neocortex. We identify 56 genes preferentially expressed in human apical and basal radial glia that lack mouse orthologs. Among these, ARHGAP11B has the highest degree of radial glia-specific expression. ARHGAP11B arose from partial duplication of ARHGAP11A (which encodes a Rho guanosine triphosphatase-activating protein) on the human lineage after separation from the chimpanzee lineage. Expression of ARHGAP11B in embryonic mouse neocortex promotes basal progenitor generation and self-renewal and can increase cortical plate area and induce gyrification. Hence, ARHGAP11B may have contributed to evolutionary expansion of human neocortex., (Copyright © 2015, American Association for the Advancement of Science.)

Published
2015
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6. Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Author

Patel, Yash, Shin, Jean, Abé, Christoph, Agartz, Ingrid, Alloza, Clara, Alnæs, Dag, Ambrogi, Sonia, Antonucci, Linda A, Arango, Celso, Arolt, Volker, Auzias, Guillaume, Ayesa-Arriola, Rosa, Banaj, Nerisa, Banaschewski, Tobias, Bandeira, Cibele, Başgöze, Zeynep, Cupertino, Renata Basso, Bau, Claiton HD, Bauer, Jochen, Baumeister, Sarah, Bernardoni, Fabio, Bertolino, Alessandro, Bonnin, Caterina Del Mar, Brandeis, Daniel, Brem, Silvia, Bruggemann, Jason, Bülow, Robin, Bustillo, Juan R, Calderoni, Sara, Calvo, Rosa, Canales-Rodríguez, Erick J, Cannon, Dara M, Carmona, Susanna, Carr, Vaughan J, Catts, Stanley V, Chenji, Sneha, Chew, Qian Hui, Coghill, David, Connolly, Colm G, Conzelmann, Annette, Craven, Alexander R, Crespo-Facorro, Benedicto, Cullen, Kathryn, Dahl, Andreas, Dannlowski, Udo, Davey, Christopher G, Deruelle, Christine, Díaz-Caneja, Covadonga M, Dohm, Katharina, Ehrlich, Stefan, Epstein, Jeffery, Erwin-Grabner, Tracy, Eyler, Lisa T, Fedor, Jennifer, Fitzgerald, Jacqueline, Foran, William, Ford, Judith M, Fortea, Lydia, Fuentes-Claramonte, Paola, Fullerton, Janice, Furlong, Lisa, Gallagher, Louise, Gao, Bingchen, Gao, Si, Goikolea, Jose M, Gotlib, Ian, Goya-Maldonado, Roberto, Grabe, Hans J, Green, Melissa, Grevet, Eugenio H, Groenewold, Nynke A, Grotegerd, Dominik, Gruber, Oliver, Haavik, Jan, Hahn, Tim, Harrison, Ben J, Heindel, Walter, Henskens, Frans, Heslenfeld, Dirk J, Hilland, Eva, Hoekstra, Pieter J, Hohmann, Sarah, Holz, Nathalie, Howells, Fleur M, Ipser, Jonathan C, Jahanshad, Neda, Jakobi, Babette, Jansen, Andreas, Janssen, Joost, Jonassen, Rune, Kaiser, Anna, Kaleda, Vasiliy, Karantonis, James, King, Joseph A, Kircher, Tilo, Kochunov, Peter, Koopowitz, Sheri-Michelle, Landén, Mikael, Landrø, Nils Inge, and Lawrie, Stephen

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Psychology, Schizophrenia, Neurosciences, Brain Disorders, Biotechnology, Perinatal Period - Conditions Originating in Perinatal Period, Infant Mortality, Pediatric, Serious Mental Illness, Intellectual and Developmental Disabilities (IDD), Genetics, Mental Health, Preterm, Low Birth Weight and Health of the Newborn, 2.3 Psychological, social and economic factors, Aetiology, 2.1 Biological and endogenous factors, Neurological, Mental health, Reproductive health and childbirth, Good Health and Well Being, Attention Deficit Disorder with Hyperactivity, Autism Spectrum Disorder, Bipolar Disorder, Cerebral Cortex, Child, Depressive Disorder, Major, Female, Humans, Infant, Newborn, Magnetic Resonance Imaging, Pregnancy, Premature Birth, Cortical growth, Cortical surface area, Mental illness, Neurodevelopment, Neurogenesis, Psychiatric disorders, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry, Biological sciences, Biomedical and clinical sciences
Abstract

BackgroundMorphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life.MethodsInterregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed.ResultsAcross the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth.ConclusionsOur findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from typical brain development during pregnancy.

Published
2022

7. MicroRNA profiling of mouse cortical progenitors and neurons reveals miR-486-5p as a regulator of neurogenesis.

Author

Dori, Martina, Cavalli, Daniel, Lesche, Mathias, Massalini, Simone, Abdullah Alieh, Leila Haj, de Toledo, Beatriz Cardoso, Khudayberdiev, Sharof, Schratt, Gerhard, Dahl, Andreas, and Calegari, Federico

Subjects
NEURAL stem cells, DEVELOPMENTAL neurobiology, NON-coding RNA, MICRORNA, NEURAL development, MICE, NEURONS
Abstract

MicroRNAs (miRNAs) are short (~22 nt) single-stranded non-coding RNAs that regulate gene expression at the post-transcriptional level. Over recent years, many studies have extensively characterized the involvement of miRNA-mediated regulation in neurogenesis and brain development. However, a comprehensive catalog of cortical miRNAs expressed in a cell-specific manner in progenitor types of the developing mammalian cortex is still missing. Overcoming this limitation, here we exploited a double reporter mouse line previously validated by our group to allow the identification of the transcriptional signature of neurogenic commitment and provide the field with the complete atlas of miRNA expression in proliferating neural stem cells, neurogenic progenitors and newborn neurons during corticogenesis. By extending the currently known list of miRNAs expressed in the mouse brain by over twofold, our study highlights the power of cell type-specific analyses for the detection of transcripts that would otherwise be diluted out when studying bulk tissues. We further exploited our data by predicting putative miRNAs and validated the power of our approach by providing evidence for the involvement of miR-486 in brain development. [ABSTRACT FROM AUTHOR]

Published
2020
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8. microRNA profiling of mouse cortical progenitors and neurons reveals miR-486-5p as a novel regulator of neurogenesis.

Author

Dori, Martina, Cavalli, Daniel, Lesche, Mathias, Massalini, Simone, Alieh, Leila Haj Abdullah, de Toledo, Beatriz Cardoso, Khudayberdiev, Sharof, Schratt, Gerhard, Dahl, Andreas, and Calegari, Federico

Subjects
NEURAL stem cells, DEVELOPMENTAL neurobiology, NON-coding RNA, MICRORNA, NEURAL development, MICE, NEURONS
Abstract

MicroRNAs (miRNAs) are short (~22 nt) single-stranded non-coding RNAs that regulate gene expression at the post-transcriptional level. Over the past years, many studies have extensively characterized the involvement of miRNA-mediated regulation in neurogenesis and brain development. However, a comprehensive catalog of cortical miRNAs cell-specifically expressed in progenitor types of the developing mammalian cortex is still missing. Overcoming this limitation, here we exploited a double reporter mouse line previously validated by our group to allow the identification of the transcriptional signature to neurogenic commitment and provide the field with the complete atlas of miRNAs expression in proliferating neural stem cells, neurogenic progenitors and newborn neurons during corticogenesis. By extending the currently known list of miRNAs expressed in the mouse brain by over two fold, our study highlights the power of cell type-specific analyses for the detection of transcripts that would otherwise be diluted out when studying bulk tissues. We further exploited our data by predicting putative novel miRNAs and validated the power of our approach by providing novel evidence for the involvement of miR-486 as a novel player in brain development. [ABSTRACT FROM AUTHOR]

Published
2020
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9. Transcriptome sequencing during mouse brain development identifies long non-coding RNAs functionally involved in neurogenic commitment

Author

Aprea, Julieta, Prenninger, Silvia, Dori, Martina, Ghosh, Tanay, Monasor, Laura Sebastian, Wessendorf, Elke, Zocher, Sara, Massalini, Simone, Alexopoulou, Dimitra, Lesche, Mathias, Dahl, Andreas, Groszer, Matthias, Hiller, Michael, and Calegari, Federico

Subjects
Genetics and Molecular Biology (all), Immunology and Microbiology (all), Neurogenesis, Green Fluorescent Proteins, Mice, Transgenic, Splicing, Biochemistry, Article, Miat, Transgenic, Mice, Neural Stem Cells, Proto-Oncogene Proteins, Animals, Developmental, LncRNAs, Molecular Biology, Cerebral Cortex, Neurons, Neuroscience (all), Cortical development, Gene Expression Profiling, Gene Expression Regulation, Developmental, Brain, Proteins, Wnt Proteins, Alternative Splicing, Phenotype, Gene Expression Regulation, RNA, Long Noncoding, Biochemistry, Genetics and Molecular Biology (all), RNA, Long Noncoding
Abstract

Transcriptome analysis of somatic stem cells and their progeny is fundamental to identify new factors controlling proliferation versus differentiation during tissue formation. Here, we generated a combinatorial, fluorescent reporter mouse line to isolate proliferating neural stem cells, differentiating progenitors and newborn neurons that coexist as intermingled cell populations during brain development. Transcriptome sequencing revealed numerous novel long non-coding (lnc)RNAs and uncharacterized protein-coding transcripts identifying the signature of neurogenic commitment. Importantly, most lncRNAs overlapped neurogenic genes and shared with them a nearly identical expression pattern suggesting that lncRNAs control corticogenesis by tuning the expression of nearby cell fate determinants. We assessed the power of our approach by manipulating lncRNAs and protein-coding transcripts with no function in corticogenesis reported to date. This led to several evident phenotypes in neurogenic commitment and neuronal survival, indicating that our study provides a remarkably high number of uncharacterized transcripts with hitherto unsuspected roles in brain development. Finally, we focussed on one lncRNA, Miat, whose manipulation was found to trigger pleiotropic effects on brain development and aberrant splicing of Wnt7b. Hence, our study suggests that lncRNA-mediated alternative splicing of cell fate determinants controls stem-cell commitment during neurogenesis.

Published
2013

10. Virtual Ontogeny of Cortical Growth Preceding Mental Illness

Author

Yash Patel, Jean Shin, Christoph Abé, Ingrid Agartz, Clara Alloza, Dag Alnæs, Sonia Ambrogi, Linda A. Antonucci, Celso Arango, Volker Arolt, Guillaume Auzias, Rosa Ayesa-Arriola, Nerisa Banaj, Tobias Banaschewski, Cibele Bandeira, Zeynep Başgöze, Renata Basso Cupertino, Claiton H.D. Bau, Jochen Bauer, Sarah Baumeister, Fabio Bernardoni, Alessandro Bertolino, Caterina del Mar Bonnin, Daniel Brandeis, Silvia Brem, Jason Bruggemann, Robin Bülow, Juan R. Bustillo, Sara Calderoni, Rosa Calvo, Erick J. Canales-Rodríguez, Dara M. Cannon, Susanna Carmona, Vaughan J. Carr, Stanley V. Catts, Sneha Chenji, Qian Hui Chew, David Coghill, Colm G. Connolly, Annette Conzelmann, Alexander R. Craven, Benedicto Crespo-Facorro, Kathryn Cullen, Andreas Dahl, Udo Dannlowski, Christopher G. Davey, Christine Deruelle, Covadonga M. Díaz-Caneja, Katharina Dohm, Stefan Ehrlich, Jeffery Epstein, Tracy Erwin-Grabner, Lisa T. Eyler, Jennifer Fedor, Jacqueline Fitzgerald, William Foran, Judith M. Ford, Lydia Fortea, Paola Fuentes-Claramonte, Janice Fullerton, Lisa Furlong, Louise Gallagher, Bingchen Gao, Si Gao, Jose M. Goikolea, Ian Gotlib, Roberto Goya-Maldonado, Hans J. Grabe, Melissa Green, Eugenio H. Grevet, Nynke A. Groenewold, Dominik Grotegerd, Oliver Gruber, Jan Haavik, Tim Hahn, Ben J. Harrison, Walter Heindel, Frans Henskens, Dirk J. Heslenfeld, Eva Hilland, Pieter J. Hoekstra, Sarah Hohmann, Nathalie Holz, Fleur M. Howells, Jonathan C. Ipser, Neda Jahanshad, Babette Jakobi, Andreas Jansen, Joost Janssen, Rune Jonassen, Anna Kaiser, Vasiliy Kaleda, James Karantonis, Joseph A. King, Tilo Kircher, Peter Kochunov, Sheri-Michelle Koopowitz, Mikael Landén, Nils Inge Landrø, Stephen Lawrie, Irina Lebedeva, Beatriz Luna, Astri J. Lundervold, Frank P. MacMaster, Luigi A. Maglanoc, Daniel H. Mathalon, Colm McDonald, Andrew McIntosh, Susanne Meinert, Patricia T. Michie, Philip Mitchell, Ana Moreno-Alcázar, Bryan Mowry, Filippo Muratori, Leila Nabulsi, Igor Nenadić, Ruth O'Gorman Tuura, Jaap Oosterlaan, Bronwyn Overs, Christos Pantelis, Mara Parellada, Jose C. Pariente, Paul Pauli, Giulio Pergola, Francesco Maria Piarulli, Felipe Picon, Fabrizio Piras, Edith Pomarol-Clotet, Clara Pretus, Yann Quidé, Joaquim Radua, J. Antoni Ramos-Quiroga, Paul E. Rasser, Andreas Reif, Alessandra Retico, Gloria Roberts, Susan Rossell, Diego Luiz Rovaris, Katya Rubia, Matthew D. Sacchet, Josep Salavert, Raymond Salvador, Salvador Sarró, Akira Sawa, Ulrich Schall, Rodney Scott, Pierluigi Selvaggi, Tim Silk, Kang Sim, Antonin Skoch, Gianfranco Spalletta, Filip Spaniel, Dan J. Stein, Olaf Steinsträter, Aleks Stolicyn, Yoichiro Takayanagi, Leanne Tamm, Maria Tavares, Alexander Teumer, Katharina Thiel, Sophia I. Thomopoulos, David Tomecek, Alexander S. Tomyshev, Diana Tordesillas-Gutiérrez, Michela Tosetti, Anne Uhlmann, Tamsyn Van Rheenen, Javier Vazquez-Bourgón, Meike W. Vernooij, Eduard Vieta, Oscar Vilarroya, Cynthia Weickert, Thomas Weickert, Lars T. Westlye, Heather Whalley, David Willinger, Alexandra Winter, Katharina Wittfeld, Tony T. Yang, Yuliya Yoncheva, Jendé L. Zijlmans, Martine Hoogman, Barbara Franke, Daan van Rooij, Jan Buitelaar, Christopher R.K. Ching, Ole A. Andreassen, Elena Pozzi, Dick Veltman, Lianne Schmaal, Theo G.M. van Erp, Jessica Turner, F. Xavier Castellanos, Zdenka Pausova, Paul Thompson, Tomas Paus, Pediatric surgery, Anatomy and neurosciences, Psychiatry, Amsterdam Neuroscience - Brain Imaging, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, General Paediatrics, ARD - Amsterdam Reproduction and Development, Paediatrics, Radiology & Nuclear Medicine, Epidemiology, Clinical Cognitive Neuropsychiatry Research Program (CCNP), German Research Foundation, University of Münster, National Health and Medical Research Council (Australia), University of Cape Town, National Research Foundation (South Africa), Swinburne Universit, Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L. Cooper Foundation, Society of Mental Health Research, Swedish Research Council, Swedish Foundation for Strategic Research, Swedish Brain Foundation, Health Research Board (Ireland), Russian Foundation for Basic Research, University of Zurich, Pratt Foundation, Ramsay Health Care, Viertel Charitable Foundation, Schizophrenia Research Institute, European Commission, Australian Research Council, Instituto de Salud Carlos III, National Institute for Health and Care Research (US), National Institute for Health Research (UK), Ministry of Health of the Czech Republic, Bill & Melinda Gates Foundation, South African Medical Research Council, Carnegie Corporation of New York, Wellcome Trust, Medical Research Council (UK), Medical Research Scotland, Netherlands Organization for Scientific Research, Ambrogi, Sonia, Banaschewski, Tobias, Bandeira, Cibele Edom, Cupertino, Renata, Calderoni, Sara, Cannon, Dara, Carr, Vaughan, Chew, Qian Hui, Coghill, David, Cullen, Kathryn, Dahl, Andreas, Epstein, Jeffery, Foran, William, Fortea, Lydia, Fuentes-Claramonte, Paola, Fullerton, Janice M., Furlong, Lisa, Gallagher, Louise, Gao, Si, Gotlib, Ian, Haavik, Jan, Henskens, Frans, Hilland, Eva, Hoekstra, Pieter J, Howells, Fleur M, Ipser, Jonathan, Jørgensen, Jes Kristian, Karantonis, James A., Lawrie, Stephen, Research Institute of the Hospital for Sick Children and University of Toronto, University of Toronto, Departments of Physiology and Nutritional Sciences, University of Toronto, Toronto, Canada, KG Jebsen Centre for Psychosis Research, University of Oslo (UiO)-Institute of Clinical Medicine-Oslo University Hospital [Oslo], Universidad Complutense de Madrid = Complutense University of Madrid [Madrid] (UCM), Mental Health Sciences Unit, University College of London [London] (UCL), Institut de Neurosciences de la Timone (INT), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), Clinical and Behavioral Neurology - Neuroscienze e riabilitazione, IRCCS Fondazione Santa Lucia [Roma], Heidelberg University, Universidade Federal do Rio Grande do Sul [Porto Alegre] (UFRGS), Universität Heidelberg [Heidelberg] = Heidelberg University, Clinical Neuropsychology, IBBA, APH - Mental Health, Centro de Investigación Biomédica en Red de Salud Mental (CIBERSAM), Hospital Sant Joan de Déu [Barcelona], and Centro de Investigación Biomédica en Red Salud Mental [Madrid] (CIBER-SAM)

Subjects
Bipolar Disorder, Autism Spectrum Disorder, [SDV]Life Sciences [q-bio], Neurogenesis, pathology [Premature Birth], Neurodevelopment, Cortical surface area, pathology [Autism Spectrum Disorder], Cortical growth, methods [Magnetic Resonance Imaging], SDG 3 - Good Health and Well-being, Pregnancy, 130 000 Cognitive Neurology & Memory, Humans, ddc:610, Child, Biological Psychiatry, Cerebral Cortex, pathology [Depressive Disorder, Major], Depressive Disorder, Major, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Infant, Newborn, Magnetic Resonance Imaging, Mental illness, Attention Deficit Disorder with Hyperactivity, Premature Birth, genetics [Autism Spectrum Disorder], Female, Psychiatric disorders, 170 000 Motivational & Cognitive Control
Abstract

[Background]: Morphology of the human cerebral cortex differs across psychiatric disorders, with neurobiology and developmental origins mostly undetermined. Deviations in the tangential growth of the cerebral cortex during pre/perinatal periods may be reflected in individual variations in cortical surface area later in life., [Methods]: Interregional profiles of group differences in surface area between cases and controls were generated using T1-weighted magnetic resonance imaging from 27,359 individuals including those with attention-deficit/hyperactivity disorder, autism spectrum disorder, bipolar disorder, major depressive disorder, schizophrenia, and high general psychopathology (through the Child Behavior Checklist). Similarity of interregional profiles of group differences in surface area and prenatal cell-specific gene expression was assessed., [Results]: Across the 11 cortical regions, group differences in cortical area for attention-deficit/hyperactivity disorder, schizophrenia, and Child Behavior Checklist were dominant in multimodal association cortices. The same interregional profiles were also associated with interregional profiles of (prenatal) gene expression specific to proliferative cells, namely radial glia and intermediate progenitor cells (greater expression, larger difference), as well as differentiated cells, namely excitatory neurons and endothelial and mural cells (greater expression, smaller difference). Finally, these cell types were implicated in known pre/perinatal risk factors for psychosis. Genes coexpressed with radial glia were enriched with genes implicated in congenital abnormalities, birth weight, hypoxia, and starvation. Genes coexpressed with endothelial and mural genes were enriched with genes associated with maternal hypertension and preterm birth., [Conclusions]: Our findings support a neurodevelopmental model of vulnerability to mental illness whereby prenatal risk factors acting through cell-specific processes lead to deviations from typical brain development during pregnancy., This work was supported by the German Research Foundation (DFG Grant Nos. HA7070/2-2, HA7070/3, HA7070/4 [to TH]) and IZKF of the medical faculty of Münster (Grants No. Dan3/012/17 [to UD] and MzH 3/020/20 [to TH]), and NHMRC projects (Grant No. 1064643 [to BJH] and 1024570 [to CGD]). The CIAM study was supported by the University of Cape Town Research Committee, South African National Research Foundation, and the South African Medical Research Council (principal investigator [PI], Fleur M. Howells) and Grant No. R01MH117601 (to NJ). This work was funded by the German Research Foundation (Grant Nos. FOR2107 JA 1890/7-1 and FOR2107 JA 1890/7-2 [to AJ]) and Swinburne University scholarship/Australian Postgraduate Award (to JK). Collection of the COGSBD cohort was funded by the Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L Cooper Foundation, and the Society of Mental Health Research (to JK). This work was funded by the German Research Foundation (Grant Nos. FOR2107 KI588/14-1 and FOR2107 KI588/14-2 [to TK]). The St. Göran study was supported by grants from the Swedish Research Council (Grant No. 2018-02653 [to ML]), the Swedish foundation for Strategic Research (Grant No. KF10-0039 [to ML]), the Swedish Brain foundation (Grant No. FO2020-0261 [to ML]), and the Swedish Government under the LUA/ALF agreement (Grant Nos. ALF 20170019 and ALFGBG-716801 [to ML]). This work was supported by RFBR (Grant No. 20-013-00748 [to IL, AST]) and funded by the Health Research Board (Grant No. HRA_POR/2011/100 [to CM]). The Australian Schizophrenia Research Bank (ASRB) was supported by the NHMRC (Enabling Grant No. 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation, and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. This work was supported by Deutsche Forschungsgemeinschaft (Grant Nos. DFG NE 2254/2-1, NE 2254/3-1, NE2254/4-1 [to IN]), the University Research Priority Program “Integrative Human Physiology” at the University of Zurich (to ROT), an NHMRC Senior Principal Research Fellowship (Grant No. 1105825 [to CPa]), an NHMRC L3 Investigator Grant (Grant No. 1196508 [to CPa]), and NHMRC Program Grant (Grant No. 1150083 [to CPa]). ASRB was supported by the NHMRC (Enabling Grant No. 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant (Agreement No. 798181 [to GP]). ASRB was supported by the NHMRC (Enabling Grant, ID 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. The Imaging Genetics in Psychosis study was funded by Project Grants from the NHMRC (Grant Nos. APP630471 and APP1081603 [to YQ]) and the Macquarie University’s Australian Research Council (ARC) Centre of Excellence in Cognition and its Disorders (Grant No. CE110001021 [to YQ]). This work was supported by the Spanish Ministry of Science, Innovation and Universities/Economy and Competitiveness/Instituto de Salud Carlos III (Grant Nos. PI11/01766 and CPII19/00009 [to JR]), co-financed by European Regional Development Fund funds from the European Commission (“A Way of Making Europe”). ASRB was supported by the NHMRC (Enabling Grant No. 386500), the Pratt Foundation, Ramsay Health Care, the Viertel Charitable Foundation, and the Schizophrenia Research Institute. Chief investigators for ASRB were VC, US, RSc, AJ, BM, PTM, SVC, FH, and CPa. SR was supported by an NHMRC Senior Fellowship (Grant No. GNT1154651). Collection of the COGSBD cohort was funded by the Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L Cooper Foundation, and the Society of Mental Health Research (to SR). This work was supported by NIHR; MRC (to KR), NIH (Grant Nos. MH-094268, MH-105660, and MH-107730 [to ASS]). The Neuroimaging of the Children's Attention Project cohort was funded by NHMRC, Australia (Grant No. 1065895). Earlier funding for the cohort as also provided by NHMRC (Grant No. 1008522) and a grant from the Collier Foundation. The ACPU cohort was funded by NHMRC, Australia (Project Grant Nos. 384419 and 569533 [to TS]). This work was supported by research grants from the National Healthcare Group, Singapore (Grant Nos. SIG/05004, SIG/05028, and SIG /1103), and the Singapore Bioimaging Consortium (RP C009/2006 [to KS]), and the Ministry of Health, Czech Republic - conceptual development of research organization (“Institute for Clinical and Experimental Medicine - IKEM, IN 00023001” [to ASk]). This study was supported by the Italian Ministry of Health (Grant No. RC/17-18-19-20-21/A [to GS]) and Ministry of Health of the Czech Republic (Grant No. NU20-04-00393 [to FS]). The Drakenstein Child Health Study (DCHS) cohort is funded by the Bill and Melinda Gates Foundation (Grant No. OPP 1017641) and the South African Medical Research Council. This DCHS contribution was made possible in part by a grant from Carnegie Corporation of New York. The statements made and views expressed are solely the responsibility of the author (DJS). STRADL study was supported and funded by the Wellcome Trust Strategic Award “Stratifying Resilience and Depression Longitudinally” (Grant No. 104036/Z/14/Z), and the Medical Research Council Mental Health Pathfinder Award “Leveraging routinely collected and linked research data to study the causes and consequences of common mental disorders” (MRC, Grant No. MC_PC_17209). Scottish Bipolar Family Study (SBFS) was supported by National Health Service Research Scotland, through the Scottish Mental Health Research Network (www.smhrn.org.uk), who provided assistance with subject recruitment and assessments. SBFS was conducted at the Brain Research Imaging Centre (http://www.bric.ed.ac.uk), which is supported by SINAPSE (Scottish Imaging Network, a Platform for Scientific Excellence, http://www.sinapse.ac.uk). Processing of the datasets used the resources provided by the Edinburgh Compute and Data Facility (http://www.ecdf.ed.ac.uk/) (ASt). TVR was supported by an NHMRC Early Career Fellowship (Grant No. GNT1088785). Collection of the COGSBD cohort was funded by the Jack Brockhoff Foundation, University of Melbourne, Barbara Dicker Brain Sciences Foundation, Rebecca L Cooper Foundation, and the Society of Mental Health Research (to TVR). EV was supported by the Spanish Ministry of Science and Innovation (PI18/00805) integrated into the Plan Nacional de I+D+I and co-financed by the ISCIII-Subdirección General de Evaluación and the FEDER; the Instituto de Salud Carlos III; the CIBERSAM (Centro de Investigación Biomédica en Red de Salud Mental); by the CERCA Programme/Generalitat de Catalunya and the Secretaria d’Universitats i Recerca del Departament d’Economia I Coneixement (Grant No. 2017SGR1355). This study was also supported by the Departament de Salut de la Generalitat de Catalunya, Pla Estratègic de Recerca i Innovació en Salut (PERIS) 2016-2020 (Grant No. SLT006/17/00345) and the European Union Horizon 2020 research and innovation program (EU.3.1.1. Understanding health, wellbeing and disease: Grant Nos. 754907 and EU.3.1.3 [to EB]; Treating and managing disease: Grant No. 945151 [to EV]). This study was supported by the National Center for Complementary and Integrative Health (Grant Nos. R21AT009173 and R61AT009864 [to TTY]); by the National Center for Advancing Translational Sciences (CTSI), National Institutes of Health, through UCSF-CTSI (Grant No. UL1TR001872 [to TTY]); by the American Foundation for Suicide Prevention (Grant No. SRG-1-141-18 [to TTY]); by UCSF Research Evaluation and Allocation Committee (REAC) and J. Jacobson Fund (to TTY); by the NIMH (Grant No. R01MH085734 [to TTY]); and by the Brain and Behavior Research Foundation (formerly NARSAD) (to TTY). This work was supported by a personal Veni grant to MH from the Netherlands Organization for Scientific Research (NWO, Grant No. 91619115 [to MH]) and European Community’s Horizon 2020 Programme (H2020/2014 – 2020) (Grant Agreements Nos. 667302 [CoCA], 728018 [Eat2beNICE], and 847879 [PRIME] [to BF]). JBu has been supported by the EU-AIMS (European Autism Interventions) and AIMS-2-TRIALS programmes, which receive support from Innovative Medicines Initiative Joint Undertaking Grant Nos. 115300 and 777394, the resources of which are composed of financial contributions from the European Union’s FP7 and Horizon 2020 Programmes, and from the European Federation of Pharmaceutical Industries and Associations companies’ in-kind contributions, and AUTISM SPEAKS, Autistica and SFARI; and by the Horizon 2020–supported programme CANDY (Grant No. 847818 [to JBu]). This work is supported by Grant No. NIA T32AG058507 and NIH Grant No. U54EB020403 from the Big Data to Knowledge (BD2K) Program (to CRKC). ENIGMA MDD work is supported by NIH (Grant Nos. U54 EB020403 [to PT], R01 MH116147 [to PT], and R01 MH117601 [to NJ and LS]). LS was supported by an NHMRC Career Development Fellowship (Grant No. 1140764). This work was supported by the National Center for Research Resources at the NIH (Grant Nos. NIH 1 U24 RR021992 [Function Biomedical Informatics Research Network], NIH 1 U24 RR025736-01 [Biomedical Informatics Research Network Coordinating Center; http://www.birncommunity.org]). TGMvE is supported by ENIGMA’s NIH BD2K initiative (Grant No. U54 EB020403), ENIGMA Sex Differences (Grant No. R01MH116147), and ENIGMA-COINSTAC: Advanced Worldwide Transdiagnostic Analysis of Valence System Brain Circuits (Grant No. R01MH121246). This work was supported by the NIH (Grant No. R01MH121246 [to JT, Calhoun, and TGMvE]). This work was supported in part by NIH (Grant No. U54 EB020403 [to PT]).

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2022

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