Molecular pathways involved in neuronal cell adhesion and membrane scaffolding contribute to schizophrenia and bipolar disorder susceptibility
Susceptibility to schizophrenia and bipolar disorder may involve a substantial, shared contribution from thousands of common genetic variants, each of small effect. Identifying whether risk variants map to specific molecular pathways is potentially biologically informative. We report a molecular pat...
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| Veröffentlicht in: | Molecular psychiatry 2011-03, Vol.16 (3), p.286-292 |
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| creator | O'Dushlaine, C Kenny, E Heron, E Donohoe, G Gill, M Morris, D Corvin, A |
| description | Susceptibility to schizophrenia and bipolar disorder may involve a substantial, shared contribution from thousands of common genetic variants, each of small effect. Identifying whether risk variants map to specific molecular pathways is potentially biologically informative. We report a molecular pathway analysis using the single-nucleotide polymorphism (SNP) ratio test, which compares the ratio of nominally significant (
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| doi_str_mv | 10.1038/mp.2010.7 |
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P
<0.05) to nonsignificant SNPs in a given pathway to identify the ‘enrichment’ for association signals. We applied this approach to the discovery (the International Schizophrenia Consortium (
n
=6909)) and validation (Genetic Association Information Network (
n
=2729)) of schizophrenia genome-wide association study (GWAS) data sets. We investigated each of the 212 experimentally validated pathways described in the Kyoto Encyclopaedia of Genes and Genomes in the discovery sample. Nominally significant pathways were tested in the validation sample, and five pathways were found to be significant (
P
=0.03–0.001); only the cell adhesion molecule (CAM) pathway withstood conservative correction for multiple testing. Interestingly, this pathway was also significantly associated with bipolar disorder (Wellcome Trust Case Control Consortium (
n
=4847)) (
P
=0.01). At a gene level, CAM genes associated in all three samples (
NRXN1
and
CNTNAP2
), which were previously implicated in specific language disorder, autism and schizophrenia. The CAM pathway functions in neuronal cell adhesion, which is critical for synaptic formation and normal cell signaling. Similar pathways have also emerged from a pathway analysis of autism, suggesting that mechanisms involved in neuronal cell adhesion may contribute broadly to neurodevelopmental psychiatric phenotypes.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/mp.2010.7</identifier><identifier>PMID: 20157312</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/80/79 ; 631/92/1643 ; 692/699/476/1333 ; 692/699/476/1799 ; Adult and adolescent clinical studies ; Analysis ; Autism ; Behavioral Sciences ; Biological and medical sciences ; Biological Psychology ; Bipolar disorder ; Bipolar Disorder - genetics ; Bipolar disorders ; Care and treatment ; Cell adhesion & migration ; Cell adhesion molecules ; Cell Adhesion Molecules, Neuronal - genetics ; Cell signaling ; Consortia ; Datasets ; Development and progression ; Disease susceptibility ; Female ; GABA ; Genes ; Genetic aspects ; Genetic diversity ; Genetic Predisposition to Disease ; Genome-wide association studies ; Genome-Wide Association Study ; Genomes ; Health aspects ; Health risk assessment ; Humans ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Membrane Proteins - genetics ; Mental disorders ; Mood disorders ; Nerve Tissue Proteins - genetics ; Neurosciences ; original-article ; Pharmacotherapy ; Phenotypes ; Physiological aspects ; Polymorphism, Single Nucleotide - genetics ; Psychiatry ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychoses ; Risk factors ; Schizophrenia ; Schizophrenia - genetics ; Signal Transduction - genetics ; Single-nucleotide polymorphism</subject><ispartof>Molecular psychiatry, 2011-03, Vol.16 (3), p.286-292</ispartof><rights>Springer Nature Limited 2011</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2011 Nature Publishing Group</rights><rights>Nature Publishing Group 2011.</rights><rights>Copyright Nature Publishing Group Mar 2011</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c638t-e8815d4d99ac0b141fb81509f4526b780d2c89de65822fd8b68bc305f531456f3</citedby><cites>FETCH-LOGICAL-c638t-e8815d4d99ac0b141fb81509f4526b780d2c89de65822fd8b68bc305f531456f3</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.2010.7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/mp.2010.7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23948274$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20157312$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00509758$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>O'Dushlaine, C</creatorcontrib><creatorcontrib>Kenny, E</creatorcontrib><creatorcontrib>Heron, E</creatorcontrib><creatorcontrib>Donohoe, G</creatorcontrib><creatorcontrib>Gill, M</creatorcontrib><creatorcontrib>Morris, D</creatorcontrib><creatorcontrib>Corvin, A</creatorcontrib><creatorcontrib>International Schizophrenia Consortium</creatorcontrib><creatorcontrib>The International Schizophrenia Consortium</creatorcontrib><title>Molecular pathways involved in neuronal cell adhesion and membrane scaffolding contribute to schizophrenia and bipolar disorder susceptibility</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>Susceptibility to schizophrenia and bipolar disorder may involve a substantial, shared contribution from thousands of common genetic variants, each of small effect. Identifying whether risk variants map to specific molecular pathways is potentially biologically informative. We report a molecular pathway analysis using the single-nucleotide polymorphism (SNP) ratio test, which compares the ratio of nominally significant (
P
<0.05) to nonsignificant SNPs in a given pathway to identify the ‘enrichment’ for association signals. We applied this approach to the discovery (the International Schizophrenia Consortium (
n
=6909)) and validation (Genetic Association Information Network (
n
=2729)) of schizophrenia genome-wide association study (GWAS) data sets. We investigated each of the 212 experimentally validated pathways described in the Kyoto Encyclopaedia of Genes and Genomes in the discovery sample. Nominally significant pathways were tested in the validation sample, and five pathways were found to be significant (
P
=0.03–0.001); only the cell adhesion molecule (CAM) pathway withstood conservative correction for multiple testing. Interestingly, this pathway was also significantly associated with bipolar disorder (Wellcome Trust Case Control Consortium (
n
=4847)) (
P
=0.01). At a gene level, CAM genes associated in all three samples (
NRXN1
and
CNTNAP2
), which were previously implicated in specific language disorder, autism and schizophrenia. The CAM pathway functions in neuronal cell adhesion, which is critical for synaptic formation and normal cell signaling. Similar pathways have also emerged from a pathway analysis of autism, suggesting that mechanisms involved in neuronal cell adhesion may contribute broadly to neurodevelopmental psychiatric phenotypes.</description><subject>631/80/79</subject><subject>631/92/1643</subject><subject>692/699/476/1333</subject><subject>692/699/476/1799</subject><subject>Adult and adolescent clinical studies</subject><subject>Analysis</subject><subject>Autism</subject><subject>Behavioral Sciences</subject><subject>Biological and medical sciences</subject><subject>Biological Psychology</subject><subject>Bipolar disorder</subject><subject>Bipolar Disorder - genetics</subject><subject>Bipolar disorders</subject><subject>Care and treatment</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Cell Adhesion Molecules, Neuronal - genetics</subject><subject>Cell signaling</subject><subject>Consortia</subject><subject>Datasets</subject><subject>Development and progression</subject><subject>Disease susceptibility</subject><subject>Female</subject><subject>GABA</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic diversity</subject><subject>Genetic Predisposition to Disease</subject><subject>Genome-wide association studies</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Health risk assessment</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane Proteins - genetics</subject><subject>Mental disorders</subject><subject>Mood disorders</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Neurosciences</subject><subject>original-article</subject><subject>Pharmacotherapy</subject><subject>Phenotypes</subject><subject>Physiological aspects</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Psychiatry</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. 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Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Risk factors</topic><topic>Schizophrenia</topic><topic>Schizophrenia - genetics</topic><topic>Signal Transduction - genetics</topic><topic>Single-nucleotide polymorphism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>O'Dushlaine, C</creatorcontrib><creatorcontrib>Kenny, E</creatorcontrib><creatorcontrib>Heron, E</creatorcontrib><creatorcontrib>Donohoe, G</creatorcontrib><creatorcontrib>Gill, M</creatorcontrib><creatorcontrib>Morris, D</creatorcontrib><creatorcontrib>Corvin, A</creatorcontrib><creatorcontrib>International Schizophrenia Consortium</creatorcontrib><creatorcontrib>The International Schizophrenia Consortium</creatorcontrib><collection>Pascal-Francis</collection><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>ProQuest Psychology</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>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Molecular psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>O'Dushlaine, C</au><au>Kenny, E</au><au>Heron, E</au><au>Donohoe, G</au><au>Gill, M</au><au>Morris, D</au><au>Corvin, A</au><aucorp>International Schizophrenia Consortium</aucorp><aucorp>The International Schizophrenia Consortium</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular pathways involved in neuronal cell adhesion and membrane scaffolding contribute to schizophrenia and bipolar disorder susceptibility</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2011-03-01</date><risdate>2011</risdate><volume>16</volume><issue>3</issue><spage>286</spage><epage>292</epage><pages>286-292</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>Susceptibility to schizophrenia and bipolar disorder may involve a substantial, shared contribution from thousands of common genetic variants, each of small effect. Identifying whether risk variants map to specific molecular pathways is potentially biologically informative. We report a molecular pathway analysis using the single-nucleotide polymorphism (SNP) ratio test, which compares the ratio of nominally significant (
P
<0.05) to nonsignificant SNPs in a given pathway to identify the ‘enrichment’ for association signals. We applied this approach to the discovery (the International Schizophrenia Consortium (
n
=6909)) and validation (Genetic Association Information Network (
n
=2729)) of schizophrenia genome-wide association study (GWAS) data sets. We investigated each of the 212 experimentally validated pathways described in the Kyoto Encyclopaedia of Genes and Genomes in the discovery sample. Nominally significant pathways were tested in the validation sample, and five pathways were found to be significant (
P
=0.03–0.001); only the cell adhesion molecule (CAM) pathway withstood conservative correction for multiple testing. Interestingly, this pathway was also significantly associated with bipolar disorder (Wellcome Trust Case Control Consortium (
n
=4847)) (
P
=0.01). At a gene level, CAM genes associated in all three samples (
NRXN1
and
CNTNAP2
), which were previously implicated in specific language disorder, autism and schizophrenia. The CAM pathway functions in neuronal cell adhesion, which is critical for synaptic formation and normal cell signaling. Similar pathways have also emerged from a pathway analysis of autism, suggesting that mechanisms involved in neuronal cell adhesion may contribute broadly to neurodevelopmental psychiatric phenotypes.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20157312</pmid><doi>10.1038/mp.2010.7</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1359-4184 |
| ispartof | Molecular psychiatry, 2011-03, Vol.16 (3), p.286-292 |
| issn | 1359-4184 1476-5578 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals |
| subjects | 631/80/79 631/92/1643 692/699/476/1333 692/699/476/1799 Adult and adolescent clinical studies Analysis Autism Behavioral Sciences Biological and medical sciences Biological Psychology Bipolar disorder Bipolar Disorder - genetics Bipolar disorders Care and treatment Cell adhesion & migration Cell adhesion molecules Cell Adhesion Molecules, Neuronal - genetics Cell signaling Consortia Datasets Development and progression Disease susceptibility Female GABA Genes Genetic aspects Genetic diversity Genetic Predisposition to Disease Genome-wide association studies Genome-Wide Association Study Genomes Health aspects Health risk assessment Humans Male Medical sciences Medicine Medicine & Public Health Membrane Proteins - genetics Mental disorders Mood disorders Nerve Tissue Proteins - genetics Neurosciences original-article Pharmacotherapy Phenotypes Physiological aspects Polymorphism, Single Nucleotide - genetics Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Risk factors Schizophrenia Schizophrenia - genetics Signal Transduction - genetics Single-nucleotide polymorphism |
| title | Molecular pathways involved in neuronal cell adhesion and membrane scaffolding contribute to schizophrenia and bipolar disorder susceptibility |
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