Genetic TPH2 variants and the susceptibility for migraine: association of a TPH2 haplotype with migraine without aura
The serotonergic system plays a major role in the etiology of migraine. The rate-limiting enzyme in serotonin homeostasis and availability is tryptophan hydroxylase (TPH). The TPH2 isoform is responsible for the cerebral serotonin biosynthesis. To investigate the role of genetic variation in TPH2 in...
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| Veröffentlicht in: | Journal of Neural Transmission 2010-11, Vol.117 (11), p.1253-1260 |
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| container_title | Journal of Neural Transmission |
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| creator | Jung, Alexander Huge, Andreas Kuhlenbäumer, Gregor Kempt, Steffi Seehafer, Tanja Evers, Stefan Berger, Klaus Marziniak, Martin |
| description | The serotonergic system plays a major role in the etiology of migraine. The rate-limiting enzyme in serotonin homeostasis and availability is tryptophan hydroxylase (TPH). The TPH2 isoform is responsible for the cerebral serotonin biosynthesis. To investigate the role of genetic variation in
TPH2
in the pathogenesis of migraine eight haplotype tagging SNPs covering the whole
TPH2
gene where chosen using Haploview and genotyped in 503 migraineurs and 515 healthy controls. Association analysis was performed on a single SNP and haplotype basis using
χ
2
and logistic regression analysis. Single SNP analysis revealed a weak association with migraine, which did not remain after correction for multiple testing. Haplotype analyses revealed association of a haplotype with migraine without aura. Stratification by aura and triptan response did not reveal a positive association with the investigated polymorphisms. These results suggest a possible influence of genetic variation in
TPH2
in the pathogenesis of migraine. |
| doi_str_mv | 10.1007/s00702-010-0468-6 |
| format | Article |
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TPH2
in the pathogenesis of migraine eight haplotype tagging SNPs covering the whole
TPH2
gene where chosen using Haploview and genotyped in 503 migraineurs and 515 healthy controls. Association analysis was performed on a single SNP and haplotype basis using
χ
2
and logistic regression analysis. Single SNP analysis revealed a weak association with migraine, which did not remain after correction for multiple testing. Haplotype analyses revealed association of a haplotype with migraine without aura. Stratification by aura and triptan response did not reveal a positive association with the investigated polymorphisms. These results suggest a possible influence of genetic variation in
TPH2
in the pathogenesis of migraine.</description><identifier>ISSN: 0300-9564</identifier><identifier>EISSN: 1435-1463</identifier><identifier>DOI: 10.1007/s00702-010-0468-6</identifier><identifier>PMID: 20740293</identifier><identifier>CODEN: JNTRF3</identifier><language>eng</language><publisher>Vienna: Springer Vienna</publisher><subject>Adult ; Association analysis ; Basic Neurosciences ; Enzymes ; Etiology ; Female ; Genetic diversity ; Genetic Predisposition to Disease - genetics ; Genetics and Immunology - Original Article ; Genome-Wide Association Study ; Genotype ; Haplotypes ; Headache ; Homeostasis ; Humans ; Male ; Medicine ; Medicine & Public Health ; Migraine ; Migraine Disorders - genetics ; Neurology ; Neurosciences ; Polymorphism, Single Nucleotide ; Psychiatry ; Regression analysis ; Serotonin ; Single-nucleotide polymorphism ; tryptophan hydroxylase ; Tryptophan Hydroxylase - genetics</subject><ispartof>Journal of Neural Transmission, 2010-11, Vol.117 (11), p.1253-1260</ispartof><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-97b9065755f2e09af5c566791625bbfcf5cde12072ef4a029ca8468f506cc763</citedby><cites>FETCH-LOGICAL-c402t-97b9065755f2e09af5c566791625bbfcf5cde12072ef4a029ca8468f506cc763</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00702-010-0468-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00702-010-0468-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20740293$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jung, Alexander</creatorcontrib><creatorcontrib>Huge, Andreas</creatorcontrib><creatorcontrib>Kuhlenbäumer, Gregor</creatorcontrib><creatorcontrib>Kempt, Steffi</creatorcontrib><creatorcontrib>Seehafer, Tanja</creatorcontrib><creatorcontrib>Evers, Stefan</creatorcontrib><creatorcontrib>Berger, Klaus</creatorcontrib><creatorcontrib>Marziniak, Martin</creatorcontrib><title>Genetic TPH2 variants and the susceptibility for migraine: association of a TPH2 haplotype with migraine without aura</title><title>Journal of Neural Transmission</title><addtitle>J Neural Transm</addtitle><addtitle>J Neural Transm (Vienna)</addtitle><description>The serotonergic system plays a major role in the etiology of migraine. The rate-limiting enzyme in serotonin homeostasis and availability is tryptophan hydroxylase (TPH). The TPH2 isoform is responsible for the cerebral serotonin biosynthesis. To investigate the role of genetic variation in
TPH2
in the pathogenesis of migraine eight haplotype tagging SNPs covering the whole
TPH2
gene where chosen using Haploview and genotyped in 503 migraineurs and 515 healthy controls. Association analysis was performed on a single SNP and haplotype basis using
χ
2
and logistic regression analysis. Single SNP analysis revealed a weak association with migraine, which did not remain after correction for multiple testing. Haplotype analyses revealed association of a haplotype with migraine without aura. Stratification by aura and triptan response did not reveal a positive association with the investigated polymorphisms. These results suggest a possible influence of genetic variation in
TPH2
in the pathogenesis of migraine.</description><subject>Adult</subject><subject>Association analysis</subject><subject>Basic Neurosciences</subject><subject>Enzymes</subject><subject>Etiology</subject><subject>Female</subject><subject>Genetic diversity</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetics and Immunology - Original Article</subject><subject>Genome-Wide Association Study</subject><subject>Genotype</subject><subject>Haplotypes</subject><subject>Headache</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Migraine</subject><subject>Migraine Disorders - genetics</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Psychiatry</subject><subject>Regression analysis</subject><subject>Serotonin</subject><subject>Single-nucleotide polymorphism</subject><subject>tryptophan hydroxylase</subject><subject>Tryptophan Hydroxylase - genetics</subject><issn>0300-9564</issn><issn>1435-1463</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9P3DAQxa2qqCzQD9ALsnrhlDJO_CfurUKFrYQEh71bjtfeNcrGwXao9tvXSyiVkCouHo388_O8eQh9IfCNAIjLVA6oKyBQAeVtxT-gBaENqwjlzUe0gAagkozTY3SS0gMAECLaT-i4BkGhls0CTTd2sNkbvLpf1vhJR6-HnLAe1jhvLU5TMnbMvvO9z3vsQsQ7v4naD_Y71ikF43X2YcDBYT1rbPXYh7wfLf7t8_YVf-7ClLGeoj5DR073yX5-qadodf1zdbWsbu9ufl39uK1MGS9XUnQSOBOMudqC1I4ZxrmQhNes65wp_dqSYqa2jupiyOi27MEx4MYI3pyii1l2jOFxsimrnS9--l4PNkxJSUY5IZywd8mWMMZIQw_k1zfkQ5jiUFwUiAohZdsWiMyQiSGlaJ0ao9_puFcE1CE6NUenSnTqEJ06DHv-Ijx1O7t-ffE3qwLUM5DK1bCx8d_P_1f9A7fbo0U</recordid><startdate>20101101</startdate><enddate>20101101</enddate><creator>Jung, Alexander</creator><creator>Huge, Andreas</creator><creator>Kuhlenbäumer, Gregor</creator><creator>Kempt, Steffi</creator><creator>Seehafer, Tanja</creator><creator>Evers, Stefan</creator><creator>Berger, Klaus</creator><creator>Marziniak, Martin</creator><general>Springer Vienna</general><general>Springer Nature B.V</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>K9.</scope><scope>7X8</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20101101</creationdate><title>Genetic TPH2 variants and the susceptibility for migraine: association of a TPH2 haplotype with migraine without aura</title><author>Jung, Alexander ; Huge, Andreas ; Kuhlenbäumer, Gregor ; Kempt, Steffi ; Seehafer, Tanja ; Evers, Stefan ; Berger, Klaus ; Marziniak, Martin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-97b9065755f2e09af5c566791625bbfcf5cde12072ef4a029ca8468f506cc763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Association analysis</topic><topic>Basic Neurosciences</topic><topic>Enzymes</topic><topic>Etiology</topic><topic>Female</topic><topic>Genetic diversity</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genetics and Immunology - Original Article</topic><topic>Genome-Wide Association Study</topic><topic>Genotype</topic><topic>Haplotypes</topic><topic>Headache</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Migraine</topic><topic>Migraine Disorders - genetics</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Psychiatry</topic><topic>Regression analysis</topic><topic>Serotonin</topic><topic>Single-nucleotide polymorphism</topic><topic>tryptophan hydroxylase</topic><topic>Tryptophan Hydroxylase - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jung, Alexander</creatorcontrib><creatorcontrib>Huge, Andreas</creatorcontrib><creatorcontrib>Kuhlenbäumer, Gregor</creatorcontrib><creatorcontrib>Kempt, Steffi</creatorcontrib><creatorcontrib>Seehafer, Tanja</creatorcontrib><creatorcontrib>Evers, Stefan</creatorcontrib><creatorcontrib>Berger, Klaus</creatorcontrib><creatorcontrib>Marziniak, Martin</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 Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Journal of Neural Transmission</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jung, Alexander</au><au>Huge, Andreas</au><au>Kuhlenbäumer, Gregor</au><au>Kempt, Steffi</au><au>Seehafer, Tanja</au><au>Evers, Stefan</au><au>Berger, Klaus</au><au>Marziniak, Martin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic TPH2 variants and the susceptibility for migraine: association of a TPH2 haplotype with migraine without aura</atitle><jtitle>Journal of Neural Transmission</jtitle><stitle>J Neural Transm</stitle><addtitle>J Neural Transm (Vienna)</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>117</volume><issue>11</issue><spage>1253</spage><epage>1260</epage><pages>1253-1260</pages><issn>0300-9564</issn><eissn>1435-1463</eissn><coden>JNTRF3</coden><abstract>The serotonergic system plays a major role in the etiology of migraine. The rate-limiting enzyme in serotonin homeostasis and availability is tryptophan hydroxylase (TPH). The TPH2 isoform is responsible for the cerebral serotonin biosynthesis. To investigate the role of genetic variation in
TPH2
in the pathogenesis of migraine eight haplotype tagging SNPs covering the whole
TPH2
gene where chosen using Haploview and genotyped in 503 migraineurs and 515 healthy controls. Association analysis was performed on a single SNP and haplotype basis using
χ
2
and logistic regression analysis. Single SNP analysis revealed a weak association with migraine, which did not remain after correction for multiple testing. Haplotype analyses revealed association of a haplotype with migraine without aura. Stratification by aura and triptan response did not reveal a positive association with the investigated polymorphisms. These results suggest a possible influence of genetic variation in
TPH2
in the pathogenesis of migraine.</abstract><cop>Vienna</cop><pub>Springer Vienna</pub><pmid>20740293</pmid><doi>10.1007/s00702-010-0468-6</doi><tpages>8</tpages></addata></record> |
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| subjects | Adult Association analysis Basic Neurosciences Enzymes Etiology Female Genetic diversity Genetic Predisposition to Disease - genetics Genetics and Immunology - Original Article Genome-Wide Association Study Genotype Haplotypes Headache Homeostasis Humans Male Medicine Medicine & Public Health Migraine Migraine Disorders - genetics Neurology Neurosciences Polymorphism, Single Nucleotide Psychiatry Regression analysis Serotonin Single-nucleotide polymorphism tryptophan hydroxylase Tryptophan Hydroxylase - genetics |
| title | Genetic TPH2 variants and the susceptibility for migraine: association of a TPH2 haplotype with migraine without aura |
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