KTN1 variants and risk for attention deficit hyperactivity disorder
Individuals with attention deficit hyperactivity disorder (ADHD) show gray matter volume (GMV) reduction in the putamen. KTN1 variants may regulate kinectin 1 expression in the putamen and influence putamen structure and function. We aim to test the hypothesis that the KTN1 variants may represent a...
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| Veröffentlicht in: | American journal of medical genetics. Part B, Neuropsychiatric genetics Neuropsychiatric genetics, 2020-06, Vol.183 (4), p.234-244 |
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| creator | Luo, Xingguang Guo, Xiaoyun Tan, Yunlong Zhang, Yong Garcia‐Milian, Rolando Wang, Zhiren Shi, Jing Yu, Ting Ji, Jiawu Wang, Xiaoping Xu, Jianying Zhang, Huihao Zuo, Lingjun Lu, Lu Wang, Kesheng Li, Chiang‐Shan R. |
| description | Individuals with attention deficit hyperactivity disorder (ADHD) show gray matter volume (GMV) reduction in the putamen. KTN1 variants may regulate kinectin 1 expression in the putamen and influence putamen structure and function. We aim to test the hypothesis that the KTN1 variants may represent a genetic risk factor of ADHD. Two independent family‐based Caucasian samples were analyzed, including 922 parent–child trios (a total of 2,757 subjects with 924 ADHD children) and 735 parent–child trios (a total of 1,383 subjects with 613 ADHD children). The association between ADHD and a total of 143 KTN1 SNPs was analyzed in the first sample, and the nominally‐significant (p |
| doi_str_mv | 10.1002/ajmg.b.32782 |
| format | Article |
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KTN1 variants may regulate kinectin 1 expression in the putamen and influence putamen structure and function. We aim to test the hypothesis that the KTN1 variants may represent a genetic risk factor of ADHD. Two independent family‐based Caucasian samples were analyzed, including 922 parent–child trios (a total of 2,757 subjects with 924 ADHD children) and 735 parent–child trios (a total of 1,383 subjects with 613 ADHD children). The association between ADHD and a total of 143 KTN1 SNPs was analyzed in the first sample, and the nominally‐significant (p < .05) risk SNPs were classified into independent haplotype blocks. All SNPs, including imputed SNPs within these blocks, and haplotypes across each block, were explored for replication of associations in both samples. The potential biological functions of all risk SNPs were predicted using a series of bioinformatics analyses, their regulatory effects on the putamen volumes were tested, and the KTN1 mRNA expression was examined in three independent human putamen tissue samples. We found that fifteen SNPs were nominally associated with ADHD (p < .05) in the first sample, and three of them remained significant even after correction for multiple testing (1.3 × 10−10 ≤ p ≤ 1.2 × 10−4; α = 2.5 × 10−3). These 15 risk SNPs were located in five haplotype blocks, and 13 SNPs within four of these blocks were associated with ADHD in the second sample. Six haplotypes within these blocks were also significantly (1.2 × 10−7 ≤ p ≤ .009) associated with ADHD in these samples. These risk variants were located in disease‐related transposons and/or transcription‐related functional regions. Major alleles of these risk variants significantly increased putamen volumes. Finally, KTN1 mRNA was significantly expressed in putamen across three independent cohorts. We concluded that the KTN1 variants were significantly associated with ADHD. KTN1 may play a functional role in the development of ADHD.</description><identifier>ISSN: 1552-4841</identifier><identifier>EISSN: 1552-485X</identifier><identifier>DOI: 10.1002/ajmg.b.32782</identifier><identifier>PMID: 32190980</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley & Sons, Inc</publisher><subject>ADHD ; Adolescent ; Alleles ; Attention Deficit Disorder with Hyperactivity - genetics ; Attention deficit hyperactivity disorder ; Bioinformatics ; Child ; Children ; Computational Biology - methods ; Family Health ; Female ; Gene expression ; Genetic Predisposition to Disease ; Genetic Variation ; Genetics ; Genotype ; Gray Matter - physiopathology ; gray matter volume ; Haplotypes ; Haplotypes - genetics ; Humans ; KTN1 ; Male ; Membrane Proteins - genetics ; Polymorphism, Single Nucleotide ; Putamen ; Risk ; Risk factors ; Single-nucleotide polymorphism ; Structure-function relationships ; Substantia grisea ; Transcription ; transposon ; Transposons</subject><ispartof>American journal of medical genetics. Part B, Neuropsychiatric genetics, 2020-06, Vol.183 (4), p.234-244</ispartof><rights>2020 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4572-ab49c6eb67368a365b8cacd0d3b4b7ccd0513ae0661080ed0be8839a5c87b1143</citedby><cites>FETCH-LOGICAL-c4572-ab49c6eb67368a365b8cacd0d3b4b7ccd0513ae0661080ed0be8839a5c87b1143</cites><orcidid>0000-0003-3585-042X ; 0000-0003-1557-566X</orcidid></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.32782$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fajmg.b.32782$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32190980$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Luo, Xingguang</creatorcontrib><creatorcontrib>Guo, Xiaoyun</creatorcontrib><creatorcontrib>Tan, Yunlong</creatorcontrib><creatorcontrib>Zhang, Yong</creatorcontrib><creatorcontrib>Garcia‐Milian, Rolando</creatorcontrib><creatorcontrib>Wang, Zhiren</creatorcontrib><creatorcontrib>Shi, Jing</creatorcontrib><creatorcontrib>Yu, Ting</creatorcontrib><creatorcontrib>Ji, Jiawu</creatorcontrib><creatorcontrib>Wang, Xiaoping</creatorcontrib><creatorcontrib>Xu, Jianying</creatorcontrib><creatorcontrib>Zhang, Huihao</creatorcontrib><creatorcontrib>Zuo, Lingjun</creatorcontrib><creatorcontrib>Lu, Lu</creatorcontrib><creatorcontrib>Wang, Kesheng</creatorcontrib><creatorcontrib>Li, Chiang‐Shan R.</creatorcontrib><title>KTN1 variants and risk for attention deficit hyperactivity disorder</title><title>American journal of medical genetics. Part B, Neuropsychiatric genetics</title><addtitle>Am J Med Genet B Neuropsychiatr Genet</addtitle><description>Individuals with attention deficit hyperactivity disorder (ADHD) show gray matter volume (GMV) reduction in the putamen. KTN1 variants may regulate kinectin 1 expression in the putamen and influence putamen structure and function. We aim to test the hypothesis that the KTN1 variants may represent a genetic risk factor of ADHD. Two independent family‐based Caucasian samples were analyzed, including 922 parent–child trios (a total of 2,757 subjects with 924 ADHD children) and 735 parent–child trios (a total of 1,383 subjects with 613 ADHD children). The association between ADHD and a total of 143 KTN1 SNPs was analyzed in the first sample, and the nominally‐significant (p < .05) risk SNPs were classified into independent haplotype blocks. All SNPs, including imputed SNPs within these blocks, and haplotypes across each block, were explored for replication of associations in both samples. The potential biological functions of all risk SNPs were predicted using a series of bioinformatics analyses, their regulatory effects on the putamen volumes were tested, and the KTN1 mRNA expression was examined in three independent human putamen tissue samples. We found that fifteen SNPs were nominally associated with ADHD (p < .05) in the first sample, and three of them remained significant even after correction for multiple testing (1.3 × 10−10 ≤ p ≤ 1.2 × 10−4; α = 2.5 × 10−3). These 15 risk SNPs were located in five haplotype blocks, and 13 SNPs within four of these blocks were associated with ADHD in the second sample. Six haplotypes within these blocks were also significantly (1.2 × 10−7 ≤ p ≤ .009) associated with ADHD in these samples. These risk variants were located in disease‐related transposons and/or transcription‐related functional regions. Major alleles of these risk variants significantly increased putamen volumes. Finally, KTN1 mRNA was significantly expressed in putamen across three independent cohorts. We concluded that the KTN1 variants were significantly associated with ADHD. KTN1 may play a functional role in the development of ADHD.</description><subject>ADHD</subject><subject>Adolescent</subject><subject>Alleles</subject><subject>Attention Deficit Disorder with Hyperactivity - genetics</subject><subject>Attention deficit hyperactivity disorder</subject><subject>Bioinformatics</subject><subject>Child</subject><subject>Children</subject><subject>Computational Biology - methods</subject><subject>Family Health</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic Variation</subject><subject>Genetics</subject><subject>Genotype</subject><subject>Gray Matter - physiopathology</subject><subject>gray matter volume</subject><subject>Haplotypes</subject><subject>Haplotypes - genetics</subject><subject>Humans</subject><subject>KTN1</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Putamen</subject><subject>Risk</subject><subject>Risk factors</subject><subject>Single-nucleotide polymorphism</subject><subject>Structure-function relationships</subject><subject>Substantia grisea</subject><subject>Transcription</subject><subject>transposon</subject><subject>Transposons</subject><issn>1552-4841</issn><issn>1552-485X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1PAjEQhhujEURvns0mXjwIttvdbXsxQaL4gXrBxFvTdgsUly22uxj-vUWQqAcPk5mkT57M9AXgGMEOgjC-ENPZuCM7OCY03gFNlKZxO6Hp6-52TlADHHg_hRDDlJB90MAxYpBR2AS9h-ETihbCGVFWPhJlHjnj36KRdZGoKl1WxpZRrkdGmSqaLOfaCVWZhamWUW68dbl2h2BvJAqvjza9BV5uroe92_bguX_X6w7aKklJ3BYyYSrTMiM4owJnqaRKqBzmWCaSqDClCAsNswxBCnUOpaYUM5EqSiRCCW6By7V3XsuZzlVYzomCz52ZCbfkVhj--6U0Ez62C07i8FMZC4KzjcDZ91r7is-MV7ooRKlt7XmMCYOIJRQF9PQPOrW1K8N5gWIMhkIkUOdrSjnrvdOj7TII8lU6fJUOl_wrnYCf_DxgC3_HEYBkDXyYQi__lfHu_WP_au39BMBDnHE</recordid><startdate>202006</startdate><enddate>202006</enddate><creator>Luo, Xingguang</creator><creator>Guo, Xiaoyun</creator><creator>Tan, Yunlong</creator><creator>Zhang, Yong</creator><creator>Garcia‐Milian, Rolando</creator><creator>Wang, Zhiren</creator><creator>Shi, Jing</creator><creator>Yu, Ting</creator><creator>Ji, Jiawu</creator><creator>Wang, Xiaoping</creator><creator>Xu, Jianying</creator><creator>Zhang, Huihao</creator><creator>Zuo, Lingjun</creator><creator>Lu, Lu</creator><creator>Wang, Kesheng</creator><creator>Li, Chiang‐Shan R.</creator><general>John Wiley & Sons, Inc</general><general>Wiley Subscription Services, Inc</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>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3585-042X</orcidid><orcidid>https://orcid.org/0000-0003-1557-566X</orcidid></search><sort><creationdate>202006</creationdate><title>KTN1 variants and risk for attention deficit hyperactivity disorder</title><author>Luo, Xingguang ; Guo, Xiaoyun ; Tan, Yunlong ; Zhang, Yong ; Garcia‐Milian, Rolando ; Wang, Zhiren ; Shi, Jing ; Yu, Ting ; Ji, Jiawu ; Wang, Xiaoping ; Xu, Jianying ; Zhang, Huihao ; Zuo, Lingjun ; Lu, Lu ; Wang, Kesheng ; Li, Chiang‐Shan R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4572-ab49c6eb67368a365b8cacd0d3b4b7ccd0513ae0661080ed0be8839a5c87b1143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>ADHD</topic><topic>Adolescent</topic><topic>Alleles</topic><topic>Attention Deficit Disorder with Hyperactivity - genetics</topic><topic>Attention deficit hyperactivity disorder</topic><topic>Bioinformatics</topic><topic>Child</topic><topic>Children</topic><topic>Computational Biology - methods</topic><topic>Family Health</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic Variation</topic><topic>Genetics</topic><topic>Genotype</topic><topic>Gray Matter - physiopathology</topic><topic>gray matter volume</topic><topic>Haplotypes</topic><topic>Haplotypes - genetics</topic><topic>Humans</topic><topic>KTN1</topic><topic>Male</topic><topic>Membrane Proteins - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Putamen</topic><topic>Risk</topic><topic>Risk factors</topic><topic>Single-nucleotide polymorphism</topic><topic>Structure-function relationships</topic><topic>Substantia grisea</topic><topic>Transcription</topic><topic>transposon</topic><topic>Transposons</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Luo, Xingguang</creatorcontrib><creatorcontrib>Guo, Xiaoyun</creatorcontrib><creatorcontrib>Tan, Yunlong</creatorcontrib><creatorcontrib>Zhang, Yong</creatorcontrib><creatorcontrib>Garcia‐Milian, Rolando</creatorcontrib><creatorcontrib>Wang, Zhiren</creatorcontrib><creatorcontrib>Shi, Jing</creatorcontrib><creatorcontrib>Yu, Ting</creatorcontrib><creatorcontrib>Ji, Jiawu</creatorcontrib><creatorcontrib>Wang, Xiaoping</creatorcontrib><creatorcontrib>Xu, Jianying</creatorcontrib><creatorcontrib>Zhang, Huihao</creatorcontrib><creatorcontrib>Zuo, Lingjun</creatorcontrib><creatorcontrib>Lu, Lu</creatorcontrib><creatorcontrib>Wang, Kesheng</creatorcontrib><creatorcontrib>Li, Chiang‐Shan R.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of medical genetics. Part B, Neuropsychiatric genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Luo, Xingguang</au><au>Guo, Xiaoyun</au><au>Tan, Yunlong</au><au>Zhang, Yong</au><au>Garcia‐Milian, Rolando</au><au>Wang, Zhiren</au><au>Shi, Jing</au><au>Yu, Ting</au><au>Ji, Jiawu</au><au>Wang, Xiaoping</au><au>Xu, Jianying</au><au>Zhang, Huihao</au><au>Zuo, Lingjun</au><au>Lu, Lu</au><au>Wang, Kesheng</au><au>Li, Chiang‐Shan R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>KTN1 variants and risk for attention deficit hyperactivity disorder</atitle><jtitle>American journal of medical genetics. Part B, Neuropsychiatric genetics</jtitle><addtitle>Am J Med Genet B Neuropsychiatr Genet</addtitle><date>2020-06</date><risdate>2020</risdate><volume>183</volume><issue>4</issue><spage>234</spage><epage>244</epage><pages>234-244</pages><issn>1552-4841</issn><eissn>1552-485X</eissn><abstract>Individuals with attention deficit hyperactivity disorder (ADHD) show gray matter volume (GMV) reduction in the putamen. KTN1 variants may regulate kinectin 1 expression in the putamen and influence putamen structure and function. We aim to test the hypothesis that the KTN1 variants may represent a genetic risk factor of ADHD. Two independent family‐based Caucasian samples were analyzed, including 922 parent–child trios (a total of 2,757 subjects with 924 ADHD children) and 735 parent–child trios (a total of 1,383 subjects with 613 ADHD children). The association between ADHD and a total of 143 KTN1 SNPs was analyzed in the first sample, and the nominally‐significant (p < .05) risk SNPs were classified into independent haplotype blocks. All SNPs, including imputed SNPs within these blocks, and haplotypes across each block, were explored for replication of associations in both samples. The potential biological functions of all risk SNPs were predicted using a series of bioinformatics analyses, their regulatory effects on the putamen volumes were tested, and the KTN1 mRNA expression was examined in three independent human putamen tissue samples. We found that fifteen SNPs were nominally associated with ADHD (p < .05) in the first sample, and three of them remained significant even after correction for multiple testing (1.3 × 10−10 ≤ p ≤ 1.2 × 10−4; α = 2.5 × 10−3). These 15 risk SNPs were located in five haplotype blocks, and 13 SNPs within four of these blocks were associated with ADHD in the second sample. Six haplotypes within these blocks were also significantly (1.2 × 10−7 ≤ p ≤ .009) associated with ADHD in these samples. These risk variants were located in disease‐related transposons and/or transcription‐related functional regions. Major alleles of these risk variants significantly increased putamen volumes. Finally, KTN1 mRNA was significantly expressed in putamen across three independent cohorts. We concluded that the KTN1 variants were significantly associated with ADHD. KTN1 may play a functional role in the development of ADHD.</abstract><cop>Hoboken, USA</cop><pub>John Wiley & Sons, Inc</pub><pmid>32190980</pmid><doi>10.1002/ajmg.b.32782</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-3585-042X</orcidid><orcidid>https://orcid.org/0000-0003-1557-566X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | ADHD Adolescent Alleles Attention Deficit Disorder with Hyperactivity - genetics Attention deficit hyperactivity disorder Bioinformatics Child Children Computational Biology - methods Family Health Female Gene expression Genetic Predisposition to Disease Genetic Variation Genetics Genotype Gray Matter - physiopathology gray matter volume Haplotypes Haplotypes - genetics Humans KTN1 Male Membrane Proteins - genetics Polymorphism, Single Nucleotide Putamen Risk Risk factors Single-nucleotide polymorphism Structure-function relationships Substantia grisea Transcription transposon Transposons |
| title | KTN1 variants and risk for attention deficit hyperactivity disorder |
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