High rate of disease-related copy number variations in childhood onset schizophrenia

Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia. Childhood onset schizophrenia (COS), defined as onset before the age of 13 years, is a rare and severe form of the disorder, with more striking ar...

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Published inMolecular psychiatry Vol. 19; no. 5; pp. 568 - 572
Main Authors Ahn, K, Gotay, N, Andersen, T M, Anvari, A A, Gochman, P, Lee, Y, Sanders, S, Guha, S, Darvasi, A, Glessner, J T, Hakonarson, H, Lencz, T, State, M W, Shugart, Y Y, Rapoport, J L
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.05.2014
Nature Publishing Group
Subjects
631/208/726/649/2157
692/699/375/366
692/699/476/1799
Adult
Adult and adolescent clinical studies
Autism
Behavioral Sciences
Biological and medical sciences
Biological Psychology
Child
Child Development Disorders, Pervasive - genetics
Child psychopathology
Children
Copy number
DNA Copy Number Variations
Epilepsy
Female
Gene mapping
Genetic aspects
Genetic Pleiotropy
Genetic variability
Genetic variation
Genetics
Genomes
Genomics
Genotyping
Genotyping Techniques
Hallucinations
Humans
Intellectual disabilities
Male
Medical sciences
Medicine
Medicine & Public Health
Mental disorders
Mental health
Neurodevelopmental disorders
Neurosciences
original-article
Patients
Pharmacotherapy
Physiological aspects
Polymorphism
Polymorphism, Single Nucleotide
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychoses
Risk factors
Schizophrenia
Schizophrenia - genetics
Schizophrenia, Childhood - genetics
Sequence Deletion
Siblings
United States
United States > US
CNV
genetics
schizophrenia
neurodevelopment
Psychosis
Age of onset
Copy number
Schizophrenia
Genetics
Infantile experience
Genetic determinism
Polymorphism
Online AccessGet full text

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Abstract Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia. Childhood onset schizophrenia (COS), defined as onset before the age of 13 years, is a rare and severe form of the disorder, with more striking array of prepsychotic developmental disorders and abnormalities in brain development. Because of the well-known phenotypic variability associated with pathogenic CNVs, we conducted whole genome genotyping to detect CNVs and then focused on a group of 46 rare CNVs that had well-documented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or ID. We evaluated 126 COS probands, 69 of which also had a healthy full sibling. When COS probands were compared with their matched related controls, significantly more affected individuals carried disease-related CNVs ( P =0.017). Moreover, COS probands showed a higher rate than that found in AOS probands ( P <0.0001). A total of 15 (11.9%) subjects exhibited at least one such CNV and four of these subjects (26.7%) had two. Five of 15 (4.0% of the sample) had a 2.5–3 Mb deletion mapping to 22q11.2, a rate higher than that reported for adult onset (0.3–1%) ( P <0.001) or autism spectrum disorder and, indeed, the highest rate reported for any clinical population to date. For one COS subject, a duplication found at 22q13.3 had previously only been associated with autism, and for four patients CNVs at 8q11.2, 10q22.3, 16p11.2 and 17q21.3 had only previously been associated with ID. Taken together, these findings support the well-known pleiotropic effects of these CNVs suggesting shared abnormalities early in brain development. Clinically, broad CNV-based population screening is needed to assess their overall clinical burden.
AbstractList Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia. Childhood onset schizophrenia (COS), defined as onset before the age of 13 years, is a rare and severe form of the disorder, with more striking array of prepsychotic developmental disorders and abnormalities in brain development. Because of the well-known phenotypic variability associated with pathogenic CNVs, we conducted whole genome genotyping to detect CNVs and then focused on a group of 46 rare CNVs that had well-documented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or ID. We evaluated 126 COS probands, 69 of which also had a healthy full sibling. When COS probands were compared with their matched related controls, significantly more affected individuals carried disease-related CNVs (P - = 0.017). Moreover, COS probands showed a higher rate than that found in AOS probands (P<0.0001). A total of 15 (11.9%) subjects exhibited at least one such CNV and four of these subjects (26.7%) had two. Five of 15 (4.0% of the sample) had a 2.5-3 Mb deletion mapping to 22q11.2, a rate higher than that reported for adult onset (0.3-1%) (P<0.001) or autism spectrum disorder and, indeed, the highest rate reported for any clinical population to date. For one COS subject, a duplication found at 22q13.3 had previously only been associated with autism, and for four patients CNVs at 8q11.2, 10q22.3, 16p11.2 and 17q21.3 had only previously been associated with ID. Taken together, these findings support the well-known pleiotropic effects of these CNVs suggesting shared abnormalities early in brain development. Clinically, broad CNV-based population screening is needed to assess their overall clinical burden. Molecular Psychiatry (2014) 19, 568-572; doi: 10.1038/mp.2013.59; published online 21 May 2013 Keywords: CNV; genetics; neurodevelopment; schizophrenia
Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia. Childhood onset schizophrenia (COS), defined as onset before the age of 13 years, is a rare and severe form of the disorder, with more striking array of prepsychotic developmental disorders and abnormalities in brain development. Because of the well-known phenotypic variability associated with pathogenic CNVs, we conducted whole genome genotyping to detect CNVs and then focused on a group of 46 rare CNVs that had well-documented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or ID. We evaluated 126 COS probands, 69 of which also had a healthy full sibling. When COS probands were compared with their matched related controls, significantly more affected individuals carried disease-related CNVs ( P = 0.017). Moreover, COS probands showed a higher rate than that found in AOS probands ( P <0.0001). A total of 15 (11.9%) subjects exhibited at least one such CNV and four of these subjects (26.7%) had two. Five of 15 (4.0% of the sample) had a 2.5–3 Mb deletion mapping to 22q11.2, a rate higher than that reported for adult onset (0.3–1%) ( P <0.001) or autism spectrum disorder and, indeed, the highest rate reported for any clinical population to date. For one COS subject, a duplication found at 22q13.3 had previously only been associated with autism, and for four patients CNVs at 8q11.2, 10q22.3, 16p11.2 and 17q21.3 had only previously been associated with ID. Taken together, these findings support the well-known pleiotropic effects of these CNVs suggesting shared abnormalities early in brain development. Clinically, broad CNV-based population screening is needed to assess their overall clinical burden.
Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia. Childhood onset schizophrenia (COS), defined as onset before the age of 13 years, is a rare and severe form of the disorder, with more striking array of prepsychotic developmental disorders and abnormalities in brain development. Because of the well-known phenotypic variability associated with pathogenic CNVs, we conducted whole genome genotyping to detect CNVs and then focused on a group of 46 rare CNVs that had well-documented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or ID. We evaluated 126 COS probands, 69 of which also had a healthy full sibling. When COS probands were compared with their matched related controls, significantly more affected individuals carried disease-related CNVs (P=0.017). Moreover, COS probands showed a higher rate than that found in AOS probands (P<0.0001). A total of 15 (11.9%) subjects exhibited at least one such CNV and four of these subjects (26.7%) had two. Five of 15 (4.0% of the sample) had a 2.5-3 Mb deletion mapping to 22q11.2, a rate higher than that reported for adult onset (0.3-1%) (P<0.001) or autism spectrum disorder and, indeed, the highest rate reported for any clinical population to date. For one COS subject, a duplication found at 22q13.3 had previously only been associated with autism, and for four patients CNVs at 8q11.2, 10q22.3, 16p11.2 and 17q21.3 had only previously been associated with ID. Taken together, these findings support the well-known pleiotropic effects of these CNVs suggesting shared abnormalities early in brain development. Clinically, broad CNV-based population screening is needed to assess their overall clinical burden.
Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia. Childhood onset schizophrenia (COS), defined as onset before the age of 13 years, is a rare and severe form of the disorder, with more striking array of prepsychotic developmental disorders and abnormalities in brain development. Because of the well-known phenotypic variability associated with pathogenic CNVs, we conducted whole genome genotyping to detect CNVs and then focused on a group of 46 rare CNVs that had well-documented risk for adult onset schizophrenia (AOS), autism, epilepsy and/or ID. We evaluated 126 COS probands, 69 of which also had a healthy full sibling. When COS probands were compared with their matched related controls, significantly more affected individuals carried disease-related CNVs (P=0.017). Moreover, COS probands showed a higher rate than that found in AOS probands (P<0.0001). A total of 15 (11.9%) subjects exhibited at least one such CNV and four of these subjects (26.7%) had two. Five of 15 (4.0% of the sample) had a 2.5-3Mb deletion mapping to 22q11.2, a rate higher than that reported for adult onset (0.3-1%) (P<0.001) or autism spectrum disorder and, indeed, the highest rate reported for any clinical population to date. For one COS subject, a duplication found at 22q13.3 had previously only been associated with autism, and for four patients CNVs at 8q11.2, 10q22.3, 16p11.2 and 17q21.3 had only previously been associated with ID. Taken together, these findings support the well-known pleiotropic effects of these CNVs suggesting shared abnormalities early in brain development. Clinically, broad CNV-based population screening is needed to assess their overall clinical burden.
Audience Academic
Author Hakonarson, H
Shugart, Y Y
Andersen, T M
Rapoport, J L
Ahn, K
Gotay, N
State, M W
Anvari, A A
Glessner, J T
Lee, Y
Darvasi, A
Lencz, T
Sanders, S
Gochman, P
Guha, S
AuthorAffiliation 1 Childhood Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
2 Program on Neurogenetics, Child Study Center, Department of Psychiatry, Department of Genetics, Yale University School of Medicine, New Haven, CT, USA
3 The Zucker Hillside Hospital, Psychiatry Research, Glen Oaks, NY, USA
6 Unit of Statistical Genomics, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA
4 Department of Genetics, The Institute of Life Sciences, The Hebrew University of Jerusalem, Givat Ram, Jerusalem, Israel
5 Center for Applied Genomics, The Children’s Hospital of Philadelphia, Philadelphia, PA, USA
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– name: 4 Department of Genetics, The Institute of Life Sciences, The Hebrew University of Jerusalem, Givat Ram, Jerusalem, Israel
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https://www.ncbi.nlm.nih.gov/pubmed/23689535$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
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Issue 5
Keywords CNV
genetics
schizophrenia
neurodevelopment
Psychosis
Age of onset
Copy number
Schizophrenia
Genetics
Infantile experience
Genetic determinism
Polymorphism
Language English
License CC BY 4.0
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PublicationTitle Molecular psychiatry
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Snippet Copy number variants (CNVs) are risk factors in neurodevelopmental disorders, including autism, epilepsy, intellectual disability (ID) and schizophrenia....
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springer
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SubjectTerms 631/208/726/649/2157
692/699/375/366
692/699/476/1799
Adult
Adult and adolescent clinical studies
Autism
Behavioral Sciences
Biological and medical sciences
Biological Psychology
Child
Child Development Disorders, Pervasive - genetics
Child psychopathology
Children
Copy number
DNA Copy Number Variations
Epilepsy
Female
Gene mapping
Genetic aspects
Genetic Pleiotropy
Genetic variability
Genetic variation
Genetics
Genomes
Genomics
Genotyping
Genotyping Techniques
Hallucinations
Humans
Intellectual disabilities
Male
Medical sciences
Medicine
Medicine & Public Health
Mental disorders
Mental health
Neurodevelopmental disorders
Neurosciences
original-article
Patients
Pharmacotherapy
Physiological aspects
Polymorphism
Polymorphism, Single Nucleotide
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychoses
Risk factors
Schizophrenia
Schizophrenia - genetics
Schizophrenia, Childhood - genetics
Sequence Deletion
Siblings
Title High rate of disease-related copy number variations in childhood onset schizophrenia
URI https://link.springer.com/article/10.1038/mp.2013.59
https://www.ncbi.nlm.nih.gov/pubmed/23689535
https://www.proquest.com/docview/1518281158
https://www.proquest.com/docview/2645761268
https://search.proquest.com/docview/1524397341
https://pubmed.ncbi.nlm.nih.gov/PMC5157161
Volume 19
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