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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| Veröffentlicht in: | Molecular psychiatry 2014-01, Vol.19 (1), p.99-107 |
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| creator | 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 |
| description | 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. |
| doi_str_mv | 10.1038/mp.2013.112 |
| format | Article |
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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.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/mp.2013.112</identifier><identifier>PMID: 23999526</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>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</subject><ispartof>Molecular psychiatry, 2014-01, Vol.19 (1), p.99-107</ispartof><rights>Macmillan Publishers Limited 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c612t-8a26e00955e45fe7a7bebec59e2ca2d45e460e51e7ba0b7185d90ab0f9a9fc293</citedby><cites>FETCH-LOGICAL-c612t-8a26e00955e45fe7a7bebec59e2ca2d45e460e51e7ba0b7185d90ab0f9a9fc293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/mp.2013.112$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/mp.2013.112$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23999526$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ellegood, J</creatorcontrib><creatorcontrib>Markx, S</creatorcontrib><creatorcontrib>Lerch, J P</creatorcontrib><creatorcontrib>Steadman, P E</creatorcontrib><creatorcontrib>Genç, C</creatorcontrib><creatorcontrib>Provenzano, F</creatorcontrib><creatorcontrib>Kushner, S A</creatorcontrib><creatorcontrib>Henkelman, R M</creatorcontrib><creatorcontrib>Karayiorgou, M</creatorcontrib><creatorcontrib>Gogos, J A</creatorcontrib><title>Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>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.</description><subject>631/208/737</subject><subject>692/699/476/1799</subject><subject>692/700/1421/65</subject><subject>Alzheimer's disease</subject><subject>Anatomy</subject><subject>Animals</subject><subject>Autism</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>Biophysics</subject><subject>Brain</subject><subject>Brain - pathology</subject><subject>Chromosome Deletion</subject><subject>Cognitive ability</subject><subject>Comparative analysis</subject><subject>Diagnosis</subject><subject>DiGeorge Syndrome - genetics</subject><subject>DiGeorge Syndrome - pathology</subject><subject>Disease</subject><subject>Disease Models, Animal</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Health risk assessment</subject><subject>Human subjects</subject><subject>Humans</subject><subject>Image Processing, Computer-Assisted</subject><subject>Magnetic Resonance Imaging</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Neurosciences</subject><subject>original-article</subject><subject>Pharmacotherapy</subject><subject>Phenotype</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Psychiatry</subject><subject>Risk factors</subject><subject>Schizophrenia</subject><subject>Third Ventricle - pathology</subject><subject>Validity</subject><issn>1359-4184</issn><issn>1476-5578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkUtr3TAQhUVoyKtZdV8M3RQau5IsWdamEEKTFEK6adZCtsf3KtiSI9mF_PuOuWmalCAYiZlvjjgzhHxgtGC0rL-OU8EpKwvG-B45YkJVuZSqfofvUupcsFockuOU7ildi_KAHPJSay15dUSub2GJwXo7h9G1dsimLfgwP06QMuczm41hSYCxgyELfTZvIeP8gbGCZ9gQ1zzMLvj3ZL-3Q4LTp_uE3F1-_3Vxnd_8vPpxcX6TtxXjc15bXgGlWkoQsgdlVQMNtFIDby3vBKYrCpKBaixtFKtlp6ltaK-t7luuyxPybac7Lc0IXQt-jnYwU3SjjY8mWGdeV7zbmk34bcpacS4lCnx-EojhYYE0m9GlFobBekCvhgnNK64wIPrpP_Q-LNGjPaQUFYwxzf9RGzuAcb4P-G-7iprzUipaSiEEUsUbFJ4OcI7BQ-8w_6rhy64Bh5xShP7ZI6NmXbwZJ7Mu3uDikf74cizP7N9NI3C2AxKW_AbiCy9v6P0BwqK1nQ</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Ellegood, J</creator><creator>Markx, S</creator><creator>Lerch, J P</creator><creator>Steadman, P E</creator><creator>Genç, C</creator><creator>Provenzano, F</creator><creator>Kushner, S A</creator><creator>Henkelman, R M</creator><creator>Karayiorgou, M</creator><creator>Gogos, J A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20140101</creationdate><title>Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c612t-8a26e00955e45fe7a7bebec59e2ca2d45e460e51e7ba0b7185d90ab0f9a9fc293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>631/208/737</topic><topic>692/699/476/1799</topic><topic>692/700/1421/65</topic><topic>Alzheimer's disease</topic><topic>Anatomy</topic><topic>Animals</topic><topic>Autism</topic><topic>Behavioral Sciences</topic><topic>Biological Psychology</topic><topic>Biophysics</topic><topic>Brain</topic><topic>Brain - pathology</topic><topic>Chromosome Deletion</topic><topic>Cognitive ability</topic><topic>Comparative analysis</topic><topic>Diagnosis</topic><topic>DiGeorge Syndrome - genetics</topic><topic>DiGeorge Syndrome - pathology</topic><topic>Disease</topic><topic>Disease Models, Animal</topic><topic>Gene mutations</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Health risk assessment</topic><topic>Human subjects</topic><topic>Humans</topic><topic>Image Processing, Computer-Assisted</topic><topic>Magnetic Resonance Imaging</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Neurosciences</topic><topic>original-article</topic><topic>Pharmacotherapy</topic><topic>Phenotype</topic><topic>Physiological aspects</topic><topic>Physiology</topic><topic>Psychiatry</topic><topic>Risk factors</topic><topic>Schizophrenia</topic><topic>Third Ventricle - pathology</topic><topic>Validity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ellegood, J</creatorcontrib><creatorcontrib>Markx, S</creatorcontrib><creatorcontrib>Lerch, J P</creatorcontrib><creatorcontrib>Steadman, P E</creatorcontrib><creatorcontrib>Genç, C</creatorcontrib><creatorcontrib>Provenzano, F</creatorcontrib><creatorcontrib>Kushner, S A</creatorcontrib><creatorcontrib>Henkelman, R M</creatorcontrib><creatorcontrib>Karayiorgou, M</creatorcontrib><creatorcontrib>Gogos, J A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ellegood, J</au><au>Markx, S</au><au>Lerch, J P</au><au>Steadman, P E</au><au>Genç, C</au><au>Provenzano, F</au><au>Kushner, S A</au><au>Henkelman, R M</au><au>Karayiorgou, M</au><au>Gogos, J A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2014-01-01</date><risdate>2014</risdate><volume>19</volume><issue>1</issue><spage>99</spage><epage>107</epage><pages>99-107</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><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.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23999526</pmid><doi>10.1038/mp.2013.112</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular psychiatry, 2014-01, Vol.19 (1), p.99-107 |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| 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 |
| title | Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion |
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