A high density linkage disequilibrium mapping in 14 noradrenergic genes: evidence of association between SLC6A2, ADRA1B and ADHD
Pharmacological evidence suggests the importance of noradrenergic and other monoaminergic neurotransmitters in the aetiology and treatment of attention deficit hyperactivity disorder (ADHD). Until recently, the genes of the noradrenergic pathway were not intensively investigated in ADHD compared to...
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| Veröffentlicht in: | Psychopharmacology 2013-02, Vol.225 (4), p.895-902 |
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| creator | Hawi, Ziarih Matthews, Natasha Barry, Edwina Kirley, Aiveen Wagner, Joseph Wallace, Robyn H. Heussler, Helen S. Vance, Alasdair Gill, Michael Bellgrove, Mark A. |
| description | Pharmacological evidence suggests the importance of noradrenergic and other monoaminergic neurotransmitters in the aetiology and treatment of attention deficit hyperactivity disorder (ADHD). Until recently, the genes of the noradrenergic pathway were not intensively investigated in ADHD compared to dopaminergic and serotonergic candidates. In this study, 91 SNP markers of 14 noradrenergic genes (an average density of one SNP per 4.5 kbp) were examined in ADHD samples from Ireland and Australia. Although suggestive evidence of association (nominal
p
≤ 0.05) with the genes
SLC6A2
,
ADRA1A
,
ADRA1B
and
ADRA2B
was observed, none remained significant after permutation adjustments. In contrast, haplotype analyses demonstrated a significant association between ADHD and a SLC6A2 haplotype comprising the markers rs36009, rs1800887, rs8049681, rs2242447 and rs9930182 (χ
2
= 9.39,
p
-corrected = 0.019, OR = 1.51). A rare
ADRA1B
haplotype made of six SNPs (rs2030373, rs6884105, rs756275, rs6892282, rs6888306 and rs13162302) was also associated (χ
2
= 7.79,
p
-corrected = 0.042 OR = 2.74) with the disorder. These findings provide evidence of a contribution of the noradrenaline system to the genetic aetiology of ADHD. The observed haplotype association signals may be driven by as yet unidentified functional risk variants in or around the associated regions. Functional genomic analysis is warranted to determine the biological mechanism of the observed association. |
| doi_str_mv | 10.1007/s00213-012-2875-x |
| format | Article |
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p
≤ 0.05) with the genes
SLC6A2
,
ADRA1A
,
ADRA1B
and
ADRA2B
was observed, none remained significant after permutation adjustments. In contrast, haplotype analyses demonstrated a significant association between ADHD and a SLC6A2 haplotype comprising the markers rs36009, rs1800887, rs8049681, rs2242447 and rs9930182 (χ
2
= 9.39,
p
-corrected = 0.019, OR = 1.51). A rare
ADRA1B
haplotype made of six SNPs (rs2030373, rs6884105, rs756275, rs6892282, rs6888306 and rs13162302) was also associated (χ
2
= 7.79,
p
-corrected = 0.042 OR = 2.74) with the disorder. These findings provide evidence of a contribution of the noradrenaline system to the genetic aetiology of ADHD. The observed haplotype association signals may be driven by as yet unidentified functional risk variants in or around the associated regions. Functional genomic analysis is warranted to determine the biological mechanism of the observed association.</description><identifier>ISSN: 0033-3158</identifier><identifier>EISSN: 1432-2072</identifier><identifier>DOI: 10.1007/s00213-012-2875-x</identifier><identifier>PMID: 23052569</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Adolescent ; Attention Deficit Disorder with Hyperactivity - diagnosis ; Attention Deficit Disorder with Hyperactivity - epidemiology ; Attention Deficit Disorder with Hyperactivity - genetics ; Attention deficit hyperactivity disorder ; Biomedical and Life Sciences ; Biomedicine ; Care and treatment ; Child ; Chromosome Mapping - methods ; Female ; Genes ; Genetic aspects ; Genetic Association Studies - methods ; Haplotypes ; Humans ; Linkage Disequilibrium - genetics ; Male ; Neurosciences ; Noradrenaline ; Norepinephrine Plasma Membrane Transport Proteins - genetics ; Original Investigation ; Pharmacology/Toxicology ; Polymorphism ; Polymorphism, Single Nucleotide - genetics ; Psychiatry ; Receptors, Adrenergic - genetics ; Receptors, Adrenergic, alpha-1 - genetics</subject><ispartof>Psychopharmacology, 2013-02, Vol.225 (4), p.895-902</ispartof><rights>Springer-Verlag 2012</rights><rights>COPYRIGHT 2013 Springer</rights><rights>Springer-Verlag Berlin Heidelberg 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-90cdc80c4c694d4338d8613404cb6319d8b0e41598f92c9dae9a25f11a6d20133</citedby><cites>FETCH-LOGICAL-c472t-90cdc80c4c694d4338d8613404cb6319d8b0e41598f92c9dae9a25f11a6d20133</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/s00213-012-2875-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00213-012-2875-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23052569$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hawi, Ziarih</creatorcontrib><creatorcontrib>Matthews, Natasha</creatorcontrib><creatorcontrib>Barry, Edwina</creatorcontrib><creatorcontrib>Kirley, Aiveen</creatorcontrib><creatorcontrib>Wagner, Joseph</creatorcontrib><creatorcontrib>Wallace, Robyn H.</creatorcontrib><creatorcontrib>Heussler, Helen S.</creatorcontrib><creatorcontrib>Vance, Alasdair</creatorcontrib><creatorcontrib>Gill, Michael</creatorcontrib><creatorcontrib>Bellgrove, Mark A.</creatorcontrib><title>A high density linkage disequilibrium mapping in 14 noradrenergic genes: evidence of association between SLC6A2, ADRA1B and ADHD</title><title>Psychopharmacology</title><addtitle>Psychopharmacology</addtitle><addtitle>Psychopharmacology (Berl)</addtitle><description>Pharmacological evidence suggests the importance of noradrenergic and other monoaminergic neurotransmitters in the aetiology and treatment of attention deficit hyperactivity disorder (ADHD). Until recently, the genes of the noradrenergic pathway were not intensively investigated in ADHD compared to dopaminergic and serotonergic candidates. In this study, 91 SNP markers of 14 noradrenergic genes (an average density of one SNP per 4.5 kbp) were examined in ADHD samples from Ireland and Australia. Although suggestive evidence of association (nominal
p
≤ 0.05) with the genes
SLC6A2
,
ADRA1A
,
ADRA1B
and
ADRA2B
was observed, none remained significant after permutation adjustments. In contrast, haplotype analyses demonstrated a significant association between ADHD and a SLC6A2 haplotype comprising the markers rs36009, rs1800887, rs8049681, rs2242447 and rs9930182 (χ
2
= 9.39,
p
-corrected = 0.019, OR = 1.51). A rare
ADRA1B
haplotype made of six SNPs (rs2030373, rs6884105, rs756275, rs6892282, rs6888306 and rs13162302) was also associated (χ
2
= 7.79,
p
-corrected = 0.042 OR = 2.74) with the disorder. These findings provide evidence of a contribution of the noradrenaline system to the genetic aetiology of ADHD. The observed haplotype association signals may be driven by as yet unidentified functional risk variants in or around the associated regions. Functional genomic analysis is warranted to determine the biological mechanism of the observed association.</description><subject>Adolescent</subject><subject>Attention Deficit Disorder with Hyperactivity - diagnosis</subject><subject>Attention Deficit Disorder with Hyperactivity - epidemiology</subject><subject>Attention Deficit Disorder with Hyperactivity - genetics</subject><subject>Attention deficit hyperactivity disorder</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Care and treatment</subject><subject>Child</subject><subject>Chromosome Mapping - methods</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic Association Studies - methods</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Linkage Disequilibrium - genetics</subject><subject>Male</subject><subject>Neurosciences</subject><subject>Noradrenaline</subject><subject>Norepinephrine Plasma Membrane Transport Proteins - genetics</subject><subject>Original Investigation</subject><subject>Pharmacology/Toxicology</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Psychiatry</subject><subject>Receptors, Adrenergic - genetics</subject><subject>Receptors, Adrenergic, alpha-1 - genetics</subject><issn>0033-3158</issn><issn>1432-2072</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkktv1DAUhSMEoqXwA9ggS2xYkOJrO4nNLp0CRRoJicfa8tg3qUviTO0E2h0_HQ9TngIJe-Fr-zvHvtIpiodAj4HS5lmilAEvKbCSyaYqr24VhyB43tGG3S4OKeW85FDJg-JeShc0DyHF3eKAcVqxqlaHxZeWnPv-nDgMyc_XZPDho-mROJ_wcvGD30S_jGQ0260PPfGBgCBhisZFDBh7b0mfi_Sc4CefTSySqSMmpcl6M_spkA3OnxEDebde1S17StrTty2cEBNcLs9O7xd3OjMkfHCzHhUfXr54vzor129evV6169KKhs2lotZZSa2wtRJOcC6drIELKuym5qCc3FAUUCnZKWaVM6gMqzoAUztGgfOj4snedxunywXTrEefLA6DCTgtSQNTkA05rf8DlUxyLirI6OM_0ItpiSE38o1iTAmmflK9GVD70E1zNHZnqlvOG5BVA7tnj_9C5elw9HYK2Pl8_psA9gIbp5Qidnob_WjitQaqdwHR-4DoHBC9C4i-yppHNx9eNiO6H4rvicgA2wMpX4Ue4y8d_dP1KxowwXk</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>Hawi, Ziarih</creator><creator>Matthews, Natasha</creator><creator>Barry, Edwina</creator><creator>Kirley, Aiveen</creator><creator>Wagner, Joseph</creator><creator>Wallace, Robyn H.</creator><creator>Heussler, Helen S.</creator><creator>Vance, Alasdair</creator><creator>Gill, Michael</creator><creator>Bellgrove, Mark A.</creator><general>Springer-Verlag</general><general>Springer</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>3V.</scope><scope>7QG</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>RC3</scope></search><sort><creationdate>20130201</creationdate><title>A high density linkage disequilibrium mapping in 14 noradrenergic genes: evidence of association between SLC6A2, ADRA1B and ADHD</title><author>Hawi, Ziarih ; Matthews, Natasha ; Barry, Edwina ; Kirley, Aiveen ; Wagner, Joseph ; Wallace, Robyn H. ; Heussler, Helen S. ; Vance, Alasdair ; Gill, Michael ; Bellgrove, Mark A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-90cdc80c4c694d4338d8613404cb6319d8b0e41598f92c9dae9a25f11a6d20133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adolescent</topic><topic>Attention Deficit Disorder with Hyperactivity - diagnosis</topic><topic>Attention Deficit Disorder with Hyperactivity - epidemiology</topic><topic>Attention Deficit Disorder with Hyperactivity - genetics</topic><topic>Attention deficit hyperactivity disorder</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Care and treatment</topic><topic>Child</topic><topic>Chromosome Mapping - methods</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic Association Studies - methods</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Linkage Disequilibrium - genetics</topic><topic>Male</topic><topic>Neurosciences</topic><topic>Noradrenaline</topic><topic>Norepinephrine Plasma Membrane Transport Proteins - genetics</topic><topic>Original Investigation</topic><topic>Pharmacology/Toxicology</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Psychiatry</topic><topic>Receptors, Adrenergic - genetics</topic><topic>Receptors, Adrenergic, alpha-1 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hawi, Ziarih</creatorcontrib><creatorcontrib>Matthews, Natasha</creatorcontrib><creatorcontrib>Barry, Edwina</creatorcontrib><creatorcontrib>Kirley, Aiveen</creatorcontrib><creatorcontrib>Wagner, Joseph</creatorcontrib><creatorcontrib>Wallace, Robyn H.</creatorcontrib><creatorcontrib>Heussler, Helen S.</creatorcontrib><creatorcontrib>Vance, Alasdair</creatorcontrib><creatorcontrib>Gill, Michael</creatorcontrib><creatorcontrib>Bellgrove, Mark 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>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</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>Technology Research Database</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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><jtitle>Psychopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hawi, Ziarih</au><au>Matthews, Natasha</au><au>Barry, Edwina</au><au>Kirley, Aiveen</au><au>Wagner, Joseph</au><au>Wallace, Robyn H.</au><au>Heussler, Helen S.</au><au>Vance, Alasdair</au><au>Gill, Michael</au><au>Bellgrove, Mark A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A high density linkage disequilibrium mapping in 14 noradrenergic genes: evidence of association between SLC6A2, ADRA1B and ADHD</atitle><jtitle>Psychopharmacology</jtitle><stitle>Psychopharmacology</stitle><addtitle>Psychopharmacology (Berl)</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>225</volume><issue>4</issue><spage>895</spage><epage>902</epage><pages>895-902</pages><issn>0033-3158</issn><eissn>1432-2072</eissn><abstract>Pharmacological evidence suggests the importance of noradrenergic and other monoaminergic neurotransmitters in the aetiology and treatment of attention deficit hyperactivity disorder (ADHD). Until recently, the genes of the noradrenergic pathway were not intensively investigated in ADHD compared to dopaminergic and serotonergic candidates. In this study, 91 SNP markers of 14 noradrenergic genes (an average density of one SNP per 4.5 kbp) were examined in ADHD samples from Ireland and Australia. Although suggestive evidence of association (nominal
p
≤ 0.05) with the genes
SLC6A2
,
ADRA1A
,
ADRA1B
and
ADRA2B
was observed, none remained significant after permutation adjustments. In contrast, haplotype analyses demonstrated a significant association between ADHD and a SLC6A2 haplotype comprising the markers rs36009, rs1800887, rs8049681, rs2242447 and rs9930182 (χ
2
= 9.39,
p
-corrected = 0.019, OR = 1.51). A rare
ADRA1B
haplotype made of six SNPs (rs2030373, rs6884105, rs756275, rs6892282, rs6888306 and rs13162302) was also associated (χ
2
= 7.79,
p
-corrected = 0.042 OR = 2.74) with the disorder. These findings provide evidence of a contribution of the noradrenaline system to the genetic aetiology of ADHD. The observed haplotype association signals may be driven by as yet unidentified functional risk variants in or around the associated regions. Functional genomic analysis is warranted to determine the biological mechanism of the observed association.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>23052569</pmid><doi>10.1007/s00213-012-2875-x</doi><tpages>8</tpages></addata></record> |
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| ispartof | Psychopharmacology, 2013-02, Vol.225 (4), p.895-902 |
| issn | 0033-3158 1432-2072 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals |
| subjects | Adolescent Attention Deficit Disorder with Hyperactivity - diagnosis Attention Deficit Disorder with Hyperactivity - epidemiology Attention Deficit Disorder with Hyperactivity - genetics Attention deficit hyperactivity disorder Biomedical and Life Sciences Biomedicine Care and treatment Child Chromosome Mapping - methods Female Genes Genetic aspects Genetic Association Studies - methods Haplotypes Humans Linkage Disequilibrium - genetics Male Neurosciences Noradrenaline Norepinephrine Plasma Membrane Transport Proteins - genetics Original Investigation Pharmacology/Toxicology Polymorphism Polymorphism, Single Nucleotide - genetics Psychiatry Receptors, Adrenergic - genetics Receptors, Adrenergic, alpha-1 - genetics |
| title | A high density linkage disequilibrium mapping in 14 noradrenergic genes: evidence of association between SLC6A2, ADRA1B and ADHD |
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