Genome-wide significant localization for working and spatial memory: Identifying genes for psychosis using models of cognition
It is well established that risk for developing psychosis is largely mediated by the influence of genes, but identifying precisely which genes underlie that risk has been problematic. Focusing on endophenotypes, rather than illness risk, is one solution to this problem. Impaired cognition is a well‐...
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| Veröffentlicht in: | American journal of medical genetics. Part B, Neuropsychiatric genetics Neuropsychiatric genetics, 2014-01, Vol.165B (1), p.84-95 |
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| creator | Knowles, Emma E.M. Carless, Melanie A. de Almeida, Marcio A.A. Curran, Joanne E. McKay, D. Reese Sprooten, Emma Dyer, Thomas D. Göring, Harald H. Olvera, Rene Fox, Peter Almasy, Laura Duggirala, Ravi Kent Jr, Jack W. Blangero, John Glahn, David. C. |
| description | It is well established that risk for developing psychosis is largely mediated by the influence of genes, but identifying precisely which genes underlie that risk has been problematic. Focusing on endophenotypes, rather than illness risk, is one solution to this problem. Impaired cognition is a well‐established endophenotype of psychosis. Here we aimed to characterize the genetic architecture of cognition using phenotypically detailed models as opposed to relying on general IQ or individual neuropsychological measures. In so doing we hoped to identify genes that mediate cognitive ability, which might also contribute to psychosis risk. Hierarchical factor models of genetically clustered cognitive traits were subjected to linkage analysis followed by QTL region‐specific association analyses in a sample of 1,269 Mexican American individuals from extended pedigrees. We identified four genome wide significant QTLs, two for working and two for spatial memory, and a number of plausible and interesting candidate genes. The creation of detailed models of cognition seemingly enhanced the power to detect genetic effects on cognition and provided a number of possible candidate genes for psychosis. © 2013 Wiley Periodicals, Inc. |
| doi_str_mv | 10.1002/ajmg.b.32211 |
| format | Article |
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Reese ; Sprooten, Emma ; Dyer, Thomas D. ; Göring, Harald H. ; Olvera, Rene ; Fox, Peter ; Almasy, Laura ; Duggirala, Ravi ; Kent Jr, Jack W. ; Blangero, John ; Glahn, David. C.</creator><creatorcontrib>Knowles, Emma E.M. ; Carless, Melanie A. ; de Almeida, Marcio A.A. ; Curran, Joanne E. ; McKay, D. Reese ; Sprooten, Emma ; Dyer, Thomas D. ; Göring, Harald H. ; Olvera, Rene ; Fox, Peter ; Almasy, Laura ; Duggirala, Ravi ; Kent Jr, Jack W. ; Blangero, John ; Glahn, David. C.</creatorcontrib><description>It is well established that risk for developing psychosis is largely mediated by the influence of genes, but identifying precisely which genes underlie that risk has been problematic. Focusing on endophenotypes, rather than illness risk, is one solution to this problem. Impaired cognition is a well‐established endophenotype of psychosis. Here we aimed to characterize the genetic architecture of cognition using phenotypically detailed models as opposed to relying on general IQ or individual neuropsychological measures. In so doing we hoped to identify genes that mediate cognitive ability, which might also contribute to psychosis risk. Hierarchical factor models of genetically clustered cognitive traits were subjected to linkage analysis followed by QTL region‐specific association analyses in a sample of 1,269 Mexican American individuals from extended pedigrees. We identified four genome wide significant QTLs, two for working and two for spatial memory, and a number of plausible and interesting candidate genes. The creation of detailed models of cognition seemingly enhanced the power to detect genetic effects on cognition and provided a number of possible candidate genes for psychosis. © 2013 Wiley Periodicals, Inc.</description><identifier>ISSN: 1552-4841</identifier><identifier>EISSN: 1552-485X</identifier><identifier>DOI: 10.1002/ajmg.b.32211</identifier><identifier>PMID: 24243780</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Association analysis ; Basic Helix-Loop-Helix Transcription Factors - genetics ; Cell Cycle Proteins - genetics ; Cognition ; Female ; Genetics ; Genome-Wide Association Study ; Genotype ; GWAS ; Humans ; linkage ; Male ; Memory, Short-Term ; Mexican Americans - genetics ; Middle Aged ; Neuropsychological Tests ; Psychotic Disorders - genetics ; Quantitative Trait Loci - genetics ; Risk ; schizophrenia ; Schizophrenia - genetics ; Young Adult</subject><ispartof>American journal of medical genetics. Part B, Neuropsychiatric genetics, 2014-01, Vol.165B (1), p.84-95</ispartof><rights>2013 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5281-482be4e3f79812f08f9f6fa1a5abf29eb9d1a494c056a168ac7672a0559ef4ff3</citedby><cites>FETCH-LOGICAL-c5281-482be4e3f79812f08f9f6fa1a5abf29eb9d1a494c056a168ac7672a0559ef4ff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fajmg.b.32211$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fajmg.b.32211$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24243780$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Knowles, Emma E.M.</creatorcontrib><creatorcontrib>Carless, Melanie A.</creatorcontrib><creatorcontrib>de Almeida, Marcio A.A.</creatorcontrib><creatorcontrib>Curran, Joanne E.</creatorcontrib><creatorcontrib>McKay, D. Reese</creatorcontrib><creatorcontrib>Sprooten, Emma</creatorcontrib><creatorcontrib>Dyer, Thomas D.</creatorcontrib><creatorcontrib>Göring, Harald H.</creatorcontrib><creatorcontrib>Olvera, Rene</creatorcontrib><creatorcontrib>Fox, Peter</creatorcontrib><creatorcontrib>Almasy, Laura</creatorcontrib><creatorcontrib>Duggirala, Ravi</creatorcontrib><creatorcontrib>Kent Jr, Jack W.</creatorcontrib><creatorcontrib>Blangero, John</creatorcontrib><creatorcontrib>Glahn, David. C.</creatorcontrib><title>Genome-wide significant localization for working and spatial memory: Identifying genes for psychosis using models of cognition</title><title>American journal of medical genetics. Part B, Neuropsychiatric genetics</title><addtitle>Am. J. Med. Genet</addtitle><description>It is well established that risk for developing psychosis is largely mediated by the influence of genes, but identifying precisely which genes underlie that risk has been problematic. Focusing on endophenotypes, rather than illness risk, is one solution to this problem. Impaired cognition is a well‐established endophenotype of psychosis. Here we aimed to characterize the genetic architecture of cognition using phenotypically detailed models as opposed to relying on general IQ or individual neuropsychological measures. In so doing we hoped to identify genes that mediate cognitive ability, which might also contribute to psychosis risk. Hierarchical factor models of genetically clustered cognitive traits were subjected to linkage analysis followed by QTL region‐specific association analyses in a sample of 1,269 Mexican American individuals from extended pedigrees. We identified four genome wide significant QTLs, two for working and two for spatial memory, and a number of plausible and interesting candidate genes. The creation of detailed models of cognition seemingly enhanced the power to detect genetic effects on cognition and provided a number of possible candidate genes for psychosis. © 2013 Wiley Periodicals, Inc.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Association analysis</subject><subject>Basic Helix-Loop-Helix Transcription Factors - genetics</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cognition</subject><subject>Female</subject><subject>Genetics</subject><subject>Genome-Wide Association Study</subject><subject>Genotype</subject><subject>GWAS</subject><subject>Humans</subject><subject>linkage</subject><subject>Male</subject><subject>Memory, Short-Term</subject><subject>Mexican Americans - genetics</subject><subject>Middle Aged</subject><subject>Neuropsychological Tests</subject><subject>Psychotic Disorders - genetics</subject><subject>Quantitative Trait Loci - genetics</subject><subject>Risk</subject><subject>schizophrenia</subject><subject>Schizophrenia - genetics</subject><subject>Young Adult</subject><issn>1552-4841</issn><issn>1552-485X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkk1v1DAQhiMEoh9w44wsceHQLLbjj4QDUil0KSpwWaDiYjmOvfU2sRc7YQkHfjtOt10BB8TJlt9n3pnxTJY9QnCGIMTP5KpbzupZgTFCd7J9RCnOSUkv7u7uBO1lBzGuICwg5fx-tocJJgUv4X72c66d73S-sY0G0S6dNVZJ14PWK9naH7K33gHjA9j4cGXdEkjXgLhO77IFne58GJ-Ds0a73ppx0pfa6XgdsY6juvTRRjDESel8o9sIvAHKp0ST84PsnpFt1A9vzsPs4-nrxcmb_PzD_Ozk-DxXFJco9YBrTXRheFUibGBpKsOMRJLK2uBK11WDJKmIgpRJxEqpOONYQkorbYgxxWH2Yuu7HupONyqVG2Qr1sF2MozCSyv-VJy9FEv_TRAEGSp4Mnh6YxD810HHXnQ2Kt220mk_RIFIhRnmBP0PyipGUIFZQp_8ha78EFz6iYniaViE0kQdbSkVfIxBm13dCIppB8S0A6IW1zuQ8Me_97qDb4eeALIFNrbV4z_NxPHbd_OXt775NszGXn_fhclwJRgvOBWf38_FRbXAX14tPonT4hc2aNAo</recordid><startdate>201401</startdate><enddate>201401</enddate><creator>Knowles, Emma E.M.</creator><creator>Carless, Melanie A.</creator><creator>de Almeida, Marcio A.A.</creator><creator>Curran, Joanne E.</creator><creator>McKay, D. Reese</creator><creator>Sprooten, Emma</creator><creator>Dyer, Thomas D.</creator><creator>Göring, Harald H.</creator><creator>Olvera, Rene</creator><creator>Fox, Peter</creator><creator>Almasy, Laura</creator><creator>Duggirala, Ravi</creator><creator>Kent Jr, Jack W.</creator><creator>Blangero, John</creator><creator>Glahn, David. 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Part B, Neuropsychiatric genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Knowles, Emma E.M.</au><au>Carless, Melanie A.</au><au>de Almeida, Marcio A.A.</au><au>Curran, Joanne E.</au><au>McKay, D. Reese</au><au>Sprooten, Emma</au><au>Dyer, Thomas D.</au><au>Göring, Harald H.</au><au>Olvera, Rene</au><au>Fox, Peter</au><au>Almasy, Laura</au><au>Duggirala, Ravi</au><au>Kent Jr, Jack W.</au><au>Blangero, John</au><au>Glahn, David. C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genome-wide significant localization for working and spatial memory: Identifying genes for psychosis using models of cognition</atitle><jtitle>American journal of medical genetics. Part B, Neuropsychiatric genetics</jtitle><addtitle>Am. J. Med. 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| source | MEDLINE; Wiley Journals |
| subjects | Adolescent Adult Aged Aged, 80 and over Association analysis Basic Helix-Loop-Helix Transcription Factors - genetics Cell Cycle Proteins - genetics Cognition Female Genetics Genome-Wide Association Study Genotype GWAS Humans linkage Male Memory, Short-Term Mexican Americans - genetics Middle Aged Neuropsychological Tests Psychotic Disorders - genetics Quantitative Trait Loci - genetics Risk schizophrenia Schizophrenia - genetics Young Adult |
| title | Genome-wide significant localization for working and spatial memory: Identifying genes for psychosis using models of cognition |
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