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Genetic variation in the monoamine oxidase A and serotonin transporter genes in sudden infant death syndrome

Aim The purpose of this study was to investigate common polymorphisms in the genes encoding monoamine oxidase A (MAOA) and serotonin transporter (5‐HTT) in Norwegian cases of sudden infant death syndrome (SIDS). This was done to further elucidate the role of genetic variation in these genes and SIDS...

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Published in:Acta Paediatrica 2014-04, Vol.103 (4), p.393-397
Main Authors: Opdal, Siri H, Vege, Åshild, Rognum, Torleiv O
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container_title Acta Paediatrica
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creator Opdal, Siri H
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Rognum, Torleiv O
description Aim The purpose of this study was to investigate common polymorphisms in the genes encoding monoamine oxidase A (MAOA) and serotonin transporter (5‐HTT) in Norwegian cases of sudden infant death syndrome (SIDS). This was done to further elucidate the role of genetic variation in these genes and SIDS. Methods A variable number of tandem repeat area in the promoter of the MAOA gene and rs25531 in the promoter region of the gene encoding 5‐HTT were investigated in 193 SIDS cases and 335 controls. The methods used were polymerase chain reaction, restriction fragment analysis and gel electrophoresis. Results There were no differences between SIDS cases and controls for any of the investigated polymorphisms. This was also true when male and female SIDS cases were analysed separately. Conclusion This article indicates that neither the VNTR in the promoter of the MAOA gene, nor rs25531 in the gene encoding 5‐HTT, is involved in SIDS. However, as medullary serotonergic abnormalities most likely contribute to the death in at least some SIDS cases, it is important to investigate these genes, as well as other genes involved in the serotonergic network, in more detail.
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This was done to further elucidate the role of genetic variation in these genes and SIDS. Methods A variable number of tandem repeat area in the promoter of the MAOA gene and rs25531 in the promoter region of the gene encoding 5‐HTT were investigated in 193 SIDS cases and 335 controls. The methods used were polymerase chain reaction, restriction fragment analysis and gel electrophoresis. Results There were no differences between SIDS cases and controls for any of the investigated polymorphisms. This was also true when male and female SIDS cases were analysed separately. Conclusion This article indicates that neither the VNTR in the promoter of the MAOA gene, nor rs25531 in the gene encoding 5‐HTT, is involved in SIDS. However, as medullary serotonergic abnormalities most likely contribute to the death in at least some SIDS cases, it is important to investigate these genes, as well as other genes involved in the serotonergic network, in more detail.</description><identifier>ISSN: 0803-5253</identifier><identifier>EISSN: 1651-2227</identifier><identifier>DOI: 10.1111/apa.12526</identifier><identifier>PMID: 24286237</identifier><language>eng</language><publisher>Norway: Blackwell Publishing Ltd</publisher><subject>Child, Preschool ; Female ; Genes ; Genetic Variation ; Genotype ; Humans ; Infant ; Infant, Newborn ; Male ; Minisatellite Repeats ; Monoamine Oxidase - genetics ; Monoamine oxidase A ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Serotonergic network ; Serotonin Plasma Membrane Transport Proteins - genetics ; Serotonin transporter ; SIDS ; Studies ; Sudden Infant Death - genetics ; Sudden infant death syndrome</subject><ispartof>Acta Paediatrica, 2014-04, Vol.103 (4), p.393-397</ispartof><rights>2013 Foundation Acta Pædiatrica. Published by John Wiley &amp; Sons Ltd</rights><rights>2013 Foundation Acta Paediatrica. 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This was done to further elucidate the role of genetic variation in these genes and SIDS. Methods A variable number of tandem repeat area in the promoter of the MAOA gene and rs25531 in the promoter region of the gene encoding 5‐HTT were investigated in 193 SIDS cases and 335 controls. The methods used were polymerase chain reaction, restriction fragment analysis and gel electrophoresis. Results There were no differences between SIDS cases and controls for any of the investigated polymorphisms. This was also true when male and female SIDS cases were analysed separately. Conclusion This article indicates that neither the VNTR in the promoter of the MAOA gene, nor rs25531 in the gene encoding 5‐HTT, is involved in SIDS. 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Vege, Åshild ; Rognum, Torleiv O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4616-5d80202995f1912ef1ccd14dafcaf0d754d71ae25f0f8479eb45cc026734348c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Child, Preschool</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic Variation</topic><topic>Genotype</topic><topic>Humans</topic><topic>Infant</topic><topic>Infant, Newborn</topic><topic>Male</topic><topic>Minisatellite Repeats</topic><topic>Monoamine Oxidase - genetics</topic><topic>Monoamine oxidase A</topic><topic>Polymorphism, Genetic</topic><topic>Promoter Regions, Genetic</topic><topic>Serotonergic network</topic><topic>Serotonin Plasma Membrane Transport Proteins - genetics</topic><topic>Serotonin transporter</topic><topic>SIDS</topic><topic>Studies</topic><topic>Sudden Infant Death - genetics</topic><topic>Sudden infant death syndrome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Opdal, Siri H</creatorcontrib><creatorcontrib>Vege, Åshild</creatorcontrib><creatorcontrib>Rognum, Torleiv O</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Physical Education Index</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; 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This was done to further elucidate the role of genetic variation in these genes and SIDS. Methods A variable number of tandem repeat area in the promoter of the MAOA gene and rs25531 in the promoter region of the gene encoding 5‐HTT were investigated in 193 SIDS cases and 335 controls. The methods used were polymerase chain reaction, restriction fragment analysis and gel electrophoresis. Results There were no differences between SIDS cases and controls for any of the investigated polymorphisms. This was also true when male and female SIDS cases were analysed separately. Conclusion This article indicates that neither the VNTR in the promoter of the MAOA gene, nor rs25531 in the gene encoding 5‐HTT, is involved in SIDS. 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subjects Child, Preschool
Female
Genes
Genetic Variation
Genotype
Humans
Infant
Infant, Newborn
Male
Minisatellite Repeats
Monoamine Oxidase - genetics
Monoamine oxidase A
Polymorphism, Genetic
Promoter Regions, Genetic
Serotonergic network
Serotonin Plasma Membrane Transport Proteins - genetics
Serotonin transporter
SIDS
Studies
Sudden Infant Death - genetics
Sudden infant death syndrome
title Genetic variation in the monoamine oxidase A and serotonin transporter genes in sudden infant death syndrome
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