Large-scale mapping of cortical alterations in 22q11.2 deletion syndrome: Convergence with idiopathic psychosis and effects of deletion size
The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or...
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Published in | Molecular psychiatry Vol. 25; no. 8; pp. 1822 - 1834 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.08.2020
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 1359-4184 1476-5578 1476-5578 |
DOI | 10.1038/s41380-018-0078-5 |
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Abstract | The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of variability in deletion size. To address these issues, we developed the ENIGMA (Enhancing Neuro Imaging Genetics Through Meta-Analysis) 22q11.2 Working Group, representing the largest analysis of brain structural alterations in 22q11DS to date. The imaging data were collected from 10 centers worldwide, including 474 subjects with 22q11DS (age = 18.2 ± 8.6; 46.9% female) and 315 typically developing, matched controls (age = 18.0 ± 9.2; 45.9% female). Compared to controls, 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen’s
d
= 0.61/0.65), but focal thickness reduction in temporal and cingulate cortex. Cortical surface area (SA), however, showed pervasive reductions in 22q11DS (left/right hemispheres:
d
= −1.01/−1.02). 22q11DS cases vs. controls were classified with 93.8% accuracy based on these neuroanatomic patterns. Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophrenia Working Group) revealed significant convergence of affected brain regions, particularly in fronto-temporal cortex. Finally, cortical SA was significantly greater in 22q11DS cases with smaller 1.5 Mb deletions, relative to those with typical 3 Mb deletions. We found a robust neuroanatomic signature of 22q11DS, and the first evidence that deletion size impacts brain structure. Psychotic illness in this highly penetrant deletion was associated with similar neuroanatomic abnormalities to idiopathic schizophrenia. These consistent cross-site findings highlight the homogeneity of this single genetic etiology, and support the suitability of 22q11DS as a biological model of schizophrenia. |
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AbstractList | The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of variability in deletion size. To address these issues, we developed the ENIGMA (Enhancing Neuro Imaging Genetics Through Meta-Analysis) 22q11.2 Working Group, representing the largest analysis of brain structural alterations in 22q11DS to date. The imaging data were collected from 10 centers worldwide, including 474 subjects with 22q11DS (age = 18.2 ± 8.6; 46.9% female) and 315 typically developing, matched controls (age = 18.0 ± 9.2; 45.9% female). Compared to controls, 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen’s d = 0.61/0.65), but focal thickness reduction in temporal and cingulate cortex. Cortical surface area (SA), however, showed pervasive reductions in 22q11DS (left/right hemispheres: d = −1.01/−1.02). 22q11DS cases vs. controls were classified with 93.8% accuracy based on these neuroanatomic patterns. Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophrenia Working Group) revealed significant convergence of affected brain regions, particularly in fronto-temporal cortex. Finally, cortical SA was significantly greater in 22q11DS cases with smaller 1.5 Mb deletions, relative to those with typical 3 Mb deletions. We found a robust neuroanatomic signature of 22q11DS, and the first evidence that deletion size impacts brain structure. Psychotic illness in this highly penetrant deletion was associated with similar neuroanatomic abnormalities to idiopathic schizophrenia. These consistent cross-site findings highlight the homogeneity of this single genetic etiology, and support the suitability of 22q11DS as a biological model of schizophrenia. The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of variability in deletion size. To address these issues, we developed the ENIGMA (Enhancing Neuro Imaging Genetics Through Meta-Analysis) 22q11.2 Working Group, representing the largest analysis of brain structural alterations in 22q11DS to date. The imaging data were collected from 10 centers worldwide, including 474 subjects with 22q11DS (age = 18.2 ± 8.6; 46.9% female) and 315 typically developing, matched controls (age = 18.0 ± 9.2; 45.9% female). Compared to controls, 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen's d = 0.61/0.65), but focal thickness reduction in temporal and cingulate cortex. Cortical surface area (SA), however, showed pervasive reductions in 22q11DS (left/right hemispheres: d = -1.01/-1.02). 22q11DS cases vs. controls were classified with 93.8% accuracy based on these neuroanatomic patterns. Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophrenia Working Group) revealed significant convergence of affected brain regions, particularly in fronto-temporal cortex. Finally, cortical SA was significantly greater in 22q11DS cases with smaller 1.5 Mb deletions, relative to those with typical 3 Mb deletions. We found a robust neuroanatomic signature of 22q11DS, and the first evidence that deletion size impacts brain structure. Psychotic illness in this highly penetrant deletion was associated with similar neuroanatomic abnormalities to idiopathic schizophrenia. These consistent cross-site findings highlight the homogeneity of this single genetic etiology, and support the suitability of 22q11DS as a biological model of schizophrenia. The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of variability in deletion size. To address these issues, we developed the ENIGMA (Enhancing Neuro Imaging Genetics Through Meta-Analysis) 22q11.2 Working Group, representing the largest analysis of brain structural alterations in 22q11DS to date. The imaging data were collected from 10 centers worldwide, including 474 subjects with 22q11DS (age = 18.2 ± 8.6; 46.9% female) and 315 typically developing, matched controls (age = 18.0 ± 9.2; 45.9% female). Compared to controls, 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen’s d = 0.61/0.65), but focal thickness reduction in temporal and cingulate cortex. Cortical surface area (SA), however, showed pervasive reductions in 22q11DS (left/right hemispheres: d = −1.01/−1.02). 22q11DS cases vs. controls were classified with 93.8% accuracy based on these neuroanatomic patterns. Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophrenia Working Group) revealed significant convergence of affected brain regions, particularly in fronto-temporal cortex. Finally, cortical SA was significantly greater in 22q11DS cases with smaller 1.5 Mb deletions, relative to those with typical 3 Mb deletions. We found a robust neuroanatomic signature of 22q11DS, and the first evidence that deletion size impacts brain structure. Psychotic illness in this highly penetrant deletion was associated with similar neuroanatomic abnormalities to idiopathic schizophrenia. These consistent cross-site findings highlight the homogeneity of this single genetic etiology, and support the suitability of 22q11DS as a biological model of schizophrenia. The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of variability in deletion size. To address these issues, we developed the ENIGMA (Enhancing Neuro Imaging Genetics Through Meta-Analysis) 22q11.2 Working Group, representing the largest analysis of brain structural alterations in 22q11DS to date. The imaging data were collected from 10 centers worldwide, including 474 subjects with 22q11DS (age = 18.2 [plus or minus] 8.6; 46.9% female) and 315 typically developing, matched controls (age = 18.0 [plus or minus] 9.2; 45.9% female). Compared to controls, 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen's d = 0.61/0.65), but focal thickness reduction in temporal and cingulate cortex. Cortical surface area (SA), however, showed pervasive reductions in 22q11DS (left/right hemispheres: d = -1.01/-1.02). 22q11DS cases vs. controls were classified with 93.8% accuracy based on these neuroanatomic patterns. Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophrenia Working Group) revealed significant convergence of affected brain regions, particularly in fronto-temporal cortex. Finally, cortical SA was significantly greater in 22q11DS cases with smaller 1.5 Mb deletions, relative to those with typical 3 Mb deletions. We found a robust neuroanatomic signature of 22q11DS, and the first evidence that deletion size impacts brain structure. Psychotic illness in this highly penetrant deletion was associated with similar neuroanatomic abnormalities to idiopathic schizophrenia. These consistent cross-site findings highlight the homogeneity of this single genetic etiology, and support the suitability of 22q11DS as a biological model of schizophrenia. The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of variability in deletion size. To address these issues, we developed the ENIGMA (Enhancing Neuro Imaging Genetics Through Meta-Analysis) 22q11.2 Working Group, representing the largest analysis of brain structural alterations in 22q11DS to date. The imaging data were collected from 10 centers worldwide, including 474 subjects with 22q11DS (age = 18.2 ± 8.6; 46.9% female) and 315 typically developing, matched controls (age = 18.0 ± 9.2; 45.9% female). Compared to controls, 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen's d = 0.61/0.65), but focal thickness reduction in temporal and cingulate cortex. Cortical surface area (SA), however, showed pervasive reductions in 22q11DS (left/right hemispheres: d = -1.01/-1.02). 22q11DS cases vs. controls were classified with 93.8% accuracy based on these neuroanatomic patterns. Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophrenia Working Group) revealed significant convergence of affected brain regions, particularly in fronto-temporal cortex. Finally, cortical SA was significantly greater in 22q11DS cases with smaller 1.5 Mb deletions, relative to those with typical 3 Mb deletions. We found a robust neuroanatomic signature of 22q11DS, and the first evidence that deletion size impacts brain structure. Psychotic illness in this highly penetrant deletion was associated with similar neuroanatomic abnormalities to idiopathic schizophrenia. These consistent cross-site findings highlight the homogeneity of this single genetic etiology, and support the suitability of 22q11DS as a biological model of schizophrenia.The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical changes in 22q11DS, but were generally underpowered to characterize neuroanatomic abnormalities associated with psychosis in 22q11DS, and/or neuroanatomic effects of variability in deletion size. To address these issues, we developed the ENIGMA (Enhancing Neuro Imaging Genetics Through Meta-Analysis) 22q11.2 Working Group, representing the largest analysis of brain structural alterations in 22q11DS to date. The imaging data were collected from 10 centers worldwide, including 474 subjects with 22q11DS (age = 18.2 ± 8.6; 46.9% female) and 315 typically developing, matched controls (age = 18.0 ± 9.2; 45.9% female). Compared to controls, 22q11DS individuals showed thicker cortical gray matter overall (left/right hemispheres: Cohen's d = 0.61/0.65), but focal thickness reduction in temporal and cingulate cortex. Cortical surface area (SA), however, showed pervasive reductions in 22q11DS (left/right hemispheres: d = -1.01/-1.02). 22q11DS cases vs. controls were classified with 93.8% accuracy based on these neuroanatomic patterns. Comparison of 22q11DS-psychosis to idiopathic schizophrenia (ENIGMA-Schizophrenia Working Group) revealed significant convergence of affected brain regions, particularly in fronto-temporal cortex. Finally, cortical SA was significantly greater in 22q11DS cases with smaller 1.5 Mb deletions, relative to those with typical 3 Mb deletions. We found a robust neuroanatomic signature of 22q11DS, and the first evidence that deletion size impacts brain structure. Psychotic illness in this highly penetrant deletion was associated with similar neuroanatomic abnormalities to idiopathic schizophrenia. These consistent cross-site findings highlight the homogeneity of this single genetic etiology, and support the suitability of 22q11DS as a biological model of schizophrenia. |
Audience | Academic |
Author | Vila-Rodriguez, Fidel Vorstman, Jacob Koops, Sanne Sun, Daqiang Gudbrandsen, Maria Ruparel, Kosha Moss, Hayley Lin, Amy Bassett, Anne S. Murphy, Kieran C. Jalbrzikowski, Maria van den Bree, Marianne B.M. Hansen, Laura Fremont, Wanda Antshel, Kevin M. Murphy, Clodagh M. Turner, Jessica A. Murphy, Declan van Amelsvoort, Therese Goodrich-Hunsaker, Naomi J. Qu, Xiaoping Schmitt, J. Eric Cunningham, Adam Linden, David E. J. Ching, Christopher R. K. Durdle, Courtney A. Villalon-Reina, Julio E. Bearden, Carrie E. Craig, Michael Kushan, Leila Doherty, Joanne Roalf, David R. Forsyth, Jennifer K. Campbell, Linda E. Emanuel, Beverly Bakker, Geor van Erp, Theo G. M. Daly, Eileen Thompson, Paul M. Kates, Wendy R. Fiksinski, Ania Butcher, Nancy J. McCabe, Kathryn L. Vajdi, Ariana Jonas, Rachel K. Simon, Tony J. Gur, Raquel E. Chow, Eva W. C. Owen, Michael J. McDonald-McGinn, Donna M. |
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K. organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Imaging Genetics Center, Mark and Mary Stevens Neuroimaging & Informatics Institute, Keck School of Medicine, University of Southern California, Interdepartmental Neuroscience Program, University of California, Los Angeles – sequence: 3 givenname: Amy surname: Lin fullname: Lin, Amy organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Interdepartmental Neuroscience Program, University of California, Los Angeles – sequence: 4 givenname: Jennifer K. surname: Forsyth fullname: Forsyth, Jennifer K. organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Department of Psychology, University of California, Los Angeles – sequence: 5 givenname: Leila surname: Kushan fullname: Kushan, Leila organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles – sequence: 6 givenname: Ariana surname: Vajdi fullname: Vajdi, Ariana organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles – sequence: 7 givenname: Maria surname: Jalbrzikowski fullname: Jalbrzikowski, Maria organization: Department of Psychiatry, University of Pittsburgh – sequence: 8 givenname: Laura surname: Hansen fullname: Hansen, Laura organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles – sequence: 9 givenname: Julio E. surname: Villalon-Reina fullname: Villalon-Reina, Julio E. organization: Imaging Genetics Center, Mark and Mary Stevens Neuroimaging & Informatics Institute, Keck School of Medicine, University of Southern California – sequence: 10 givenname: Xiaoping surname: Qu fullname: Qu, Xiaoping organization: Imaging Genetics Center, Mark and Mary Stevens Neuroimaging & Informatics Institute, Keck School of Medicine, University of Southern California – sequence: 11 givenname: Rachel K. surname: Jonas fullname: Jonas, Rachel K. organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Interdepartmental Neuroscience Program, University of California, Los Angeles – sequence: 12 givenname: Therese surname: van Amelsvoort fullname: van Amelsvoort, Therese organization: Department of Psychiatry & Neuropsychology, Maastricht University – sequence: 13 givenname: Geor surname: Bakker fullname: Bakker, Geor organization: Department of Psychiatry & Neuropsychology, Maastricht University – sequence: 14 givenname: Wendy R. surname: Kates fullname: Kates, Wendy R. organization: Department of Psychiatry and Behavioral Sciences, State University of New York, Upstate Medical University – sequence: 15 givenname: Kevin M. surname: Antshel fullname: Antshel, Kevin M. organization: Department of Psychology, Syracuse University – sequence: 16 givenname: Wanda surname: Fremont fullname: Fremont, Wanda organization: Department of Psychiatry and Behavioral Sciences, State University of New York, Upstate Medical University – sequence: 17 givenname: Linda E. surname: Campbell fullname: Campbell, Linda E. organization: PRC GrowUpWell, University of Newcastle, School of Psychology, University of Newcastle – sequence: 18 givenname: Kathryn L. surname: McCabe fullname: McCabe, Kathryn L. organization: School of Psychology, University of Newcastle, UC Davis MIND Institute and Department of Psychiatry and Behavioral Sciences – sequence: 19 givenname: Eileen surname: Daly fullname: Daly, Eileen organization: Sackler Institute for Translational Neurodevelopment and Department of Forensic and Neurodevelopmental Sciences, King’s College London, Institute of Psychiatry, Psychology & Neuroscience – sequence: 20 givenname: Maria surname: Gudbrandsen fullname: Gudbrandsen, Maria organization: Sackler Institute for Translational Neurodevelopment and Department of Forensic and Neurodevelopmental Sciences, King’s College London, Institute of Psychiatry, Psychology & Neuroscience – sequence: 21 givenname: Clodagh M. surname: Murphy fullname: Murphy, Clodagh M. organization: Sackler Institute for Translational Neurodevelopment and Department of Forensic and Neurodevelopmental Sciences, King’s College London, Institute of Psychiatry, Psychology & Neuroscience, Behavioural Genetics Clinic, Adult Autism Service, Behavioural and Developmental Psychiatry Clinical Academic Group, South London and Maudsley Foundation NHS Trust – sequence: 22 givenname: Declan surname: Murphy fullname: Murphy, Declan organization: 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Department of Psychiatry, University of Toronto – sequence: 25 givenname: Ania surname: Fiksinski fullname: Fiksinski, Ania organization: Hospital for Sick Children, Clinical Genetics Research Program, Centre for Addiction and Mental Health, Department of Psychiatry, University of Toronto, The Dalglish Family 22q Clinic, Department of Psychiatry, and Toronto General Research Institute, University Health Network, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health – sequence: 26 givenname: Sanne surname: Koops fullname: Koops, Sanne organization: Department of Psychiatry, Brain Center Rudolf Magnus, University Medical Center Utrecht – sequence: 27 givenname: Kosha surname: Ruparel fullname: Ruparel, Kosha organization: Department of Psychiatry, University of Pennsylvania, and the Lifespan Brain Institute, Penn Medicine and the Children’s Hospital of Philadelphia – sequence: 28 givenname: David R. surname: Roalf fullname: Roalf, David R. organization: Department of Psychiatry, University of Pennsylvania, and the Lifespan Brain Institute, Penn Medicine and the Children’s Hospital of Philadelphia – sequence: 29 givenname: Raquel E. surname: Gur fullname: Gur, Raquel E. organization: Department of Radiology, Division of Neuroradiology, Perelman School of Medicine, University of Pennsylvania, Department of Psychiatry, University of Pennsylvania, and the Lifespan Brain Institute, Penn Medicine and the Children’s Hospital of Philadelphia – sequence: 30 givenname: J. Eric surname: Schmitt fullname: Schmitt, J. Eric organization: Department of Radiology, Division of Neuroradiology, Perelman School of Medicine, University of Pennsylvania, Department of Psychiatry, University of Pennsylvania, and the Lifespan Brain Institute, Penn Medicine and the Children’s Hospital of Philadelphia – sequence: 31 givenname: Tony J. surname: Simon fullname: Simon, Tony J. organization: UC Davis MIND Institute and Department of Psychiatry and Behavioral Sciences – sequence: 32 givenname: Naomi J. surname: Goodrich-Hunsaker fullname: Goodrich-Hunsaker, Naomi J. organization: UC Davis MIND Institute and Department of Psychiatry and Behavioral Sciences, Department of Psychology, Brigham Young University – sequence: 33 givenname: Courtney A. surname: Durdle fullname: Durdle, Courtney A. organization: UC Davis MIND Institute and Department of Psychiatry and Behavioral Sciences – sequence: 34 givenname: Anne S. surname: Bassett fullname: Bassett, Anne S. organization: Clinical Genetics Research Program, Centre for Addiction and Mental Health, Department of Psychiatry, University of Toronto, The Dalglish Family 22q Clinic, Department of Psychiatry, and Toronto General Research Institute, University Health Network, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health – sequence: 35 givenname: Eva W. C. surname: Chow fullname: Chow, Eva W. C. organization: Clinical Genetics Research Program, Centre for Addiction and Mental Health, Department of Psychiatry, University of Toronto – sequence: 36 givenname: Nancy J. surname: Butcher fullname: Butcher, Nancy J. organization: Hospital for Sick Children, Clinical Genetics Research Program, Centre for Addiction and Mental Health – sequence: 37 givenname: Fidel surname: Vila-Rodriguez fullname: Vila-Rodriguez, Fidel organization: Department of Psychiatry, University of British Columbia – sequence: 38 givenname: Joanne surname: Doherty fullname: Doherty, Joanne organization: MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University – sequence: 39 givenname: Adam orcidid: 0000-0002-9791-7813 surname: Cunningham fullname: Cunningham, Adam organization: MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University – sequence: 40 givenname: Marianne B.M. surname: van den Bree fullname: van den Bree, Marianne B.M. organization: MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University – sequence: 41 givenname: David E. J. surname: Linden fullname: Linden, David E. J. organization: MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University – sequence: 42 givenname: Hayley surname: Moss fullname: Moss, Hayley organization: MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University – sequence: 43 givenname: Michael J. orcidid: 0000-0003-4798-0862 surname: Owen fullname: Owen, Michael J. organization: MRC Centre for Neuropsychiatric Genetics and Genomics, Division of Psychological Medicine and Clinical Neurosciences, Cardiff University – sequence: 44 givenname: Kieran C. surname: Murphy fullname: Murphy, Kieran C. organization: Department of Psychiatry, Royal College of Surgeons in Ireland – sequence: 45 givenname: Donna M. surname: McDonald-McGinn fullname: McDonald-McGinn, Donna M. organization: Division of Human Genetics, The Children’s Hospital of Philadelphia, Department of Pediatrics, The Perelman School of Medicine at the University of Pennsylvania, Division of Clinical Genetics, The Children’s Hospital of Philadelphia – sequence: 46 givenname: Beverly surname: Emanuel fullname: Emanuel, Beverly organization: Department of Pediatrics, The Perelman School of Medicine at the University of Pennsylvania, Division of Clinical Genetics, The Children’s Hospital of Philadelphia – sequence: 47 givenname: Theo G. M. orcidid: 0000-0002-2465-2797 surname: van Erp fullname: van Erp, Theo G. M. organization: Department of Psychiatry and Human Behavior, University of California, Irvine – sequence: 48 givenname: Jessica A. orcidid: 0000-0003-0076-8434 surname: Turner fullname: Turner, Jessica A. organization: Imaging Genetics and Neuroinformatics Lab, Department of Psychology, Georgia State University, Mind Research Network – sequence: 49 givenname: Paul M. surname: Thompson fullname: Thompson, Paul M. organization: Imaging Genetics Center, Mark and Mary Stevens Neuroimaging & Informatics Institute, Keck School of Medicine, University of Southern California, Departments of Neurology, Psychiatry, Radiology, Engineering, Pediatrics and Ophthalmology, University of Southern California – sequence: 50 givenname: Carrie E. surname: Bearden fullname: Bearden, Carrie E. email: CBearden@mednet.ucla.edu organization: Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Department of Psychology, University of California, Los Angeles |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29895892$$D View this record in MEDLINE/PubMed |
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Snippet | The 22q11.2 deletion (22q11DS) is a common chromosomal microdeletion and a potent risk factor for psychotic illness. Prior studies reported widespread cortical... |
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Title | Large-scale mapping of cortical alterations in 22q11.2 deletion syndrome: Convergence with idiopathic psychosis and effects of deletion size |
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