Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion

Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse mo...

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Published inMolecular psychiatry Vol. 19; no. 1; pp. 99 - 107
Main Authors Ellegood, J, Markx, S, Lerch, J P, Steadman, P E, Genç, C, Provenzano, F, Kushner, S A, Henkelman, R M, Karayiorgou, M, Gogos, J A
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.01.2014
Nature Publishing Group
Subjects
631/208/737
692/699/476/1799
692/700/1421/65
Alzheimer's disease
Anatomy
Animals
Autism
Behavioral Sciences
Biological Psychology
Biophysics
Brain
Brain - pathology
Chromosome Deletion
Cognitive ability
Comparative analysis
Diagnosis
DiGeorge Syndrome - genetics
DiGeorge Syndrome - pathology
Disease
Disease Models, Animal
Gene mutations
Genetic aspects
Health aspects
Health risk assessment
Human subjects
Humans
Image Processing, Computer-Assisted
Magnetic Resonance Imaging
Male
Medicine
Medicine & Public Health
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neurosciences
original-article
Pharmacotherapy
Phenotype
Physiological aspects
Physiology
Psychiatry
Risk factors
Schizophrenia
Third Ventricle - pathology
Validity
United States
New York
Canada
United States > US
schizophrenia
mouse model
22q11.2
MRI
microdeletion
Online AccessGet full text

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Abstract Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion ( Df(16)A +/− ) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A +/− mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A +/− mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A +/− mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.
AbstractList Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion (Df(16)A(+/-)) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A(+/-) mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A(+/-) mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A(+/-)mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion (Df(16)A(+/-)) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A(+/-) mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A(+/-) mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A(+/-)mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.
Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion ( Df(16)A +/− ) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A +/− mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A +/− mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A +/− mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.
Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion (Df(16)A(+/-)) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A(+/-) mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A(+/-) mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A(+/-)mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.
Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion ([Df(16)A.sup.+/-]) has previously been utilized to characterize disease- associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of [Df(16)A.sup.+/-] mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in [Df(16)A.sup.+/-] mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the [Df(16)A.sup.+/-]~ mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion- associated psychiatric and cognitive symptoms. Molecular Psychiatry (2014) 19, 99-107; doi: 10.1038/mp.2013.112; published online 3 September 2013 Keywords: 22q11.2; microdeletion; mouse model; MRI; schizophrenia
Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion (Df(16)A super(+/-)) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A super(+/-) mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A super(+/-) mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A super(+/-)mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.
Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion ( Df(16)A +/− ) has previously been utilized to characterize disease-associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type (WT) littermates. Our analysis revealed a striking similarity in the specific volumetric changes of Df(16)A +/− mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal, and cortico-limbic circuits. In addition, higher resolution compared with neuroimaging in human subjects allowed detection of previously unknown subtle local differences. The cerebellar findings in Df(16)A +/− mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the Df(16)A +/− mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion-associated psychiatric and cognitive symptoms.
Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction. Individuals with 22q11.2 deletions have a range of well-defined volumetric abnormalities in a number of critical brain structures. A mouse model of the 22q11.2 deletion ([Df(16)A.sup.+/-]) has previously been utilized to characterize disease- associated abnormalities on synaptic, cellular, neurocircuitry, and behavioral levels. We performed a high-resolution MRI analysis of mutant mice compared with wild-type littermates. Our analysis revealed a striking similarity in the specific volumetric changes of [Df(16)A.sup.+/-] mice compared with human 22q11.2 deletion carriers, including in cortico-cerebellar, cortico-striatal and cortico-limbic circuits. In addition, higher resolution magnetic resonance imaging compared with neuroimaging in human subjects allowed the detection of previously unknown subtle local differences. The cerebellar findings in [Df(16)A.sup.+/-] mice are particularly instructive as they are localized to specific areas within both the deep cerebellar nuclei and the cerebellar cortex. Our study indicates that the [Df(16)A.sup.+/-]~ mouse model recapitulates most of the hallmark neuroanatomical changes observed in 22q11.2 deletion carriers. Our findings will help guide the design and interpretation of additional complementary studies and thereby advance our understanding of the abnormal brain development underlying the emergence of 22q11.2 deletion- associated psychiatric and cognitive symptoms.
Audience Academic
Author Henkelman, R M
Ellegood, J
Kushner, S A
Genç, C
Gogos, J A
Lerch, J P
Provenzano, F
Karayiorgou, M
Markx, S
Steadman, P E
AuthorAffiliation 1 Mouse Imaging Centre, Hospital for Sick Children, Toronto, Ontario, Canada
2 Department of Medical Biophysics, University of Toronto, Toronto, Ontario Canada
5 Department of Department of Biomedical Engineering, College of Physicians and Surgeons, Columbia University, New York, New York, USA
4 Department of Psychiatry, Erasmus Medical Center, The Netherlands
3 Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, New York, USA
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– name: 1 Mouse Imaging Centre, Hospital for Sick Children, Toronto, Ontario, Canada
– name: 4 Department of Psychiatry, Erasmus Medical Center, The Netherlands
– name: 2 Department of Medical Biophysics, University of Toronto, Toronto, Ontario Canada
– name: 5 Department of Department of Biomedical Engineering, College of Physicians and Surgeons, Columbia University, New York, New York, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/23999526$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Macmillan Publishers Limited 2014
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Issue 1
Keywords schizophrenia
mouse model
22q11.2
MRI
microdeletion
Language English
License Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
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Snippet Recurrent deletions at the 22q11.2 locus have been established as a strong genetic risk factor for the development of schizophrenia and cognitive dysfunction....
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StartPage 99
SubjectTerms 631/208/737
692/699/476/1799
692/700/1421/65
Alzheimer's disease
Anatomy
Animals
Autism
Behavioral Sciences
Biological Psychology
Biophysics
Brain
Brain - pathology
Chromosome Deletion
Cognitive ability
Comparative analysis
Diagnosis
DiGeorge Syndrome - genetics
DiGeorge Syndrome - pathology
Disease
Disease Models, Animal
Gene mutations
Genetic aspects
Health aspects
Health risk assessment
Human subjects
Humans
Image Processing, Computer-Assisted
Magnetic Resonance Imaging
Male
Medicine
Medicine & Public Health
Mice
Mice, Inbred C57BL
Mice, Transgenic
Neurosciences
original-article
Pharmacotherapy
Phenotype
Physiological aspects
Physiology
Psychiatry
Risk factors
Schizophrenia
Third Ventricle - pathology
Validity
Title Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion
URI https://link.springer.com/article/10.1038/mp.2013.112
https://www.ncbi.nlm.nih.gov/pubmed/23999526
https://www.proquest.com/docview/1470411192
https://www.proquest.com/docview/1490736899
https://www.proquest.com/docview/1492627926
https://pubmed.ncbi.nlm.nih.gov/PMC3872255
Volume 19
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