Dopamine transporter SLC6A3 genotype affects cortico-striatal activity of set-shifts in Parkinson's disease.
Identifieur interne : 000643 ( PubMed/Curation ); précédent : 000642; suivant : 000644Dopamine transporter SLC6A3 genotype affects cortico-striatal activity of set-shifts in Parkinson's disease.
Auteurs : Claudine Habak [Canada] ; Anne Noreau [Canada] ; Atsuko Nagano-Saito [Canada] ; Beatriz Mejía-Constaín [Canada] ; Clotilde Degroot [Canada] ; Antonio P. Strafella [Canada] ; Sylvain Chouinard [Canada] ; Anne-Louise Lafontaine [Canada] ; Guy A. Rouleau [Canada] ; Oury Monchi [Canada]Source :
- Brain : a journal of neurology [ 1460-2156 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Dopamine Plasma Membrane Transport Proteins (genetics), Dopamine Plasma Membrane Transport Proteins (physiology), Executive Function (physiology), Female, Frontal Lobe (physiopathology), Functional Neuroimaging, Heterozygote, Homozygote, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Neostriatum (physiopathology), Parkinson Disease (genetics), Parkinson Disease (physiopathology), Polymorphism, Genetic.
- MESH :
- chemical , genetics : Dopamine Plasma Membrane Transport Proteins.
- chemical , physiology : Dopamine Plasma Membrane Transport Proteins.
- genetics : Parkinson Disease.
- physiology : Executive Function.
- physiopathology : Frontal Lobe, Neostriatum, Parkinson Disease.
- Aged, Female, Functional Neuroimaging, Heterozygote, Homozygote, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Polymorphism, Genetic.
Abstract
Parkinson's disease is a neurodegenerative condition that affects motor function along with a wide range of cognitive domains, including executive function. The hallmark of the pathology is its significant loss of nigrostriatal dopamine, which is necessary for the cortico-striatal interactions that underlie executive control. Striatal dopamine reuptake is mediated by the SLC6A3 gene (formerly named DAT1) and its polymorphisms, which have been largely overlooked in Parkinson's disease. Thirty patients (ages 53-68 years; 19 males, 11 females) at early stages of Parkinson's disease, were genotyped according to a 9-repeat (9R) or 10-repeat (10R) allele on the SLC6A3/DAT1 gene. They underwent neuropsychological assessment and functional magnetic resonance imaging while performing a set-shifting task (a computerized Wisconsin Card Sorting Task) that relies on fronto-striatal interactions. Patients homozygous on the 10R allele performed significantly better on working memory tasks than 9R-carrier patients. Most importantly, patients carrying a 9R allele exhibited less activation than their 10R homozygous counterparts in the prefrontal cortex, premotor cortex and caudate nucleus, when planning and executing a set-shift. This pattern was exacerbated for conditions that usually recruit the striatum compared to those that do not. This is the first study indicating that the SLC6A3/DAT1 genotype has a significant effect on fronto-striatal activation and performance in Parkinson's disease. This effect is stronger for conditions that engage the striatum. Longitudinal studies are warranted to assess this polymorphism's effect on the clinical evolution of patients with Parkinson's disease, especially with cognitive decline.
DOI: 10.1093/brain/awu251
PubMed: 25212851
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sortKey="Habak, Claudine" sort="Habak, Claudine" uniqKey="Habak C" first="Claudine" last="Habak">Claudine Habak</name><affiliation wicri:level="1"><nlm:affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5</wicri:regionArea></affiliation></author><author><name sortKey="Noreau, Anne" sort="Noreau, Anne" uniqKey="Noreau A" first="Anne" last="Noreau">Anne Noreau</name><affiliation wicri:level="1"><nlm:affiliation>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada 3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada 3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4</wicri:regionArea></affiliation></author><author><name sortKey="Nagano Saito, Atsuko" sort="Nagano Saito, Atsuko" uniqKey="Nagano Saito A" first="Atsuko" last="Nagano-Saito">Atsuko Nagano-Saito</name><affiliation wicri:level="1"><nlm:affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5</wicri:regionArea></affiliation></author><author><name sortKey="Mejia Constain, Beatriz" sort="Mejia Constain, Beatriz" uniqKey="Mejia Constain B" first="Beatriz" last="Mejía-Constaín">Beatriz Mejía-Constaín</name><affiliation wicri:level="1"><nlm:affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5</wicri:regionArea></affiliation></author><author><name sortKey="Degroot, Clotilde" sort="Degroot, Clotilde" uniqKey="Degroot C" first="Clotilde" last="Degroot">Clotilde Degroot</name><affiliation wicri:level="1"><nlm:affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5</wicri:regionArea></affiliation></author><author><name sortKey="Strafella, Antonio P" sort="Strafella, Antonio P" uniqKey="Strafella A" first="Antonio P" last="Strafella">Antonio P. Strafella</name><affiliation wicri:level="1"><nlm:affiliation>4 Movement Disorder Unit and E.J. Safra Parkinson Disease Program, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>4 Movement Disorder Unit and E.J. Safra Parkinson Disease Program, Toronto Western Hospital, UHN, University of Toronto, Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Chouinard, Sylvain" sort="Chouinard, Sylvain" uniqKey="Chouinard S" first="Sylvain" last="Chouinard">Sylvain Chouinard</name><affiliation wicri:level="1"><nlm:affiliation>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec</wicri:regionArea></affiliation></author><author><name sortKey="Lafontaine, Anne Louise" sort="Lafontaine, Anne Louise" uniqKey="Lafontaine A" first="Anne-Louise" last="Lafontaine">Anne-Louise Lafontaine</name><affiliation wicri:level="1"><nlm:affiliation>3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4</wicri:regionArea></affiliation></author><author><name sortKey="Rouleau, Guy A" sort="Rouleau, Guy A" uniqKey="Rouleau G" first="Guy A" last="Rouleau">Guy A. Rouleau</name><affiliation wicri:level="1"><nlm:affiliation>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada 3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada 3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4</wicri:regionArea></affiliation></author><author><name sortKey="Monchi, Oury" sort="Monchi, Oury" uniqKey="Monchi O" first="Oury" last="Monchi">Oury Monchi</name><affiliation wicri:level="1"><nlm:affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada 5 Département de Radiologie, Université de Montréal, Montréal, Québec, Canada oury.monchi@umontreal.ca.</nlm:affiliation><country wicri:rule="url">Canada</country><wicri:regionArea>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada 5 Département de Radiologie, Université de Montréal, Montréal, Québec</wicri:regionArea></affiliation></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Dopamine Plasma Membrane Transport Proteins (genetics)</term><term>Dopamine Plasma Membrane Transport Proteins (physiology)</term><term>Executive Function (physiology)</term><term>Female</term><term>Frontal Lobe (physiopathology)</term><term>Functional Neuroimaging</term><term>Heterozygote</term><term>Homozygote</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Neostriatum (physiopathology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Polymorphism, Genetic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Executive Function</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Frontal Lobe</term><term>Neostriatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Functional Neuroimaging</term><term>Heterozygote</term><term>Homozygote</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Polymorphism, Genetic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease is a neurodegenerative condition that affects motor function along with a wide range of cognitive domains, including executive function. The hallmark of the pathology is its significant loss of nigrostriatal dopamine, which is necessary for the cortico-striatal interactions that underlie executive control. Striatal dopamine reuptake is mediated by the SLC6A3 gene (formerly named DAT1) and its polymorphisms, which have been largely overlooked in Parkinson's disease. Thirty patients (ages 53-68 years; 19 males, 11 females) at early stages of Parkinson's disease, were genotyped according to a 9-repeat (9R) or 10-repeat (10R) allele on the SLC6A3/DAT1 gene. They underwent neuropsychological assessment and functional magnetic resonance imaging while performing a set-shifting task (a computerized Wisconsin Card Sorting Task) that relies on fronto-striatal interactions. Patients homozygous on the 10R allele performed significantly better on working memory tasks than 9R-carrier patients. Most importantly, patients carrying a 9R allele exhibited less activation than their 10R homozygous counterparts in the prefrontal cortex, premotor cortex and caudate nucleus, when planning and executing a set-shift. This pattern was exacerbated for conditions that usually recruit the striatum compared to those that do not. This is the first study indicating that the SLC6A3/DAT1 genotype has a significant effect on fronto-striatal activation and performance in Parkinson's disease. This effect is stronger for conditions that engage the striatum. Longitudinal studies are warranted to assess this polymorphism's effect on the clinical evolution of patients with Parkinson's disease, especially with cognitive decline.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25212851</PMID><DateCreated><Year>2014</Year><Month>10</Month><Day>25</Day></DateCreated><DateCompleted><Year>2015</Year><Month>02</Month><Day>09</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>137</Volume><Issue>Pt 11</Issue><PubDate><Year>2014</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Dopamine transporter SLC6A3 genotype affects cortico-striatal activity of set-shifts in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>3025-35</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awu251</ELocationID><Abstract><AbstractText>Parkinson's disease is a neurodegenerative condition that affects motor function along with a wide range of cognitive domains, including executive function. The hallmark of the pathology is its significant loss of nigrostriatal dopamine, which is necessary for the cortico-striatal interactions that underlie executive control. Striatal dopamine reuptake is mediated by the SLC6A3 gene (formerly named DAT1) and its polymorphisms, which have been largely overlooked in Parkinson's disease. Thirty patients (ages 53-68 years; 19 males, 11 females) at early stages of Parkinson's disease, were genotyped according to a 9-repeat (9R) or 10-repeat (10R) allele on the SLC6A3/DAT1 gene. They underwent neuropsychological assessment and functional magnetic resonance imaging while performing a set-shifting task (a computerized Wisconsin Card Sorting Task) that relies on fronto-striatal interactions. Patients homozygous on the 10R allele performed significantly better on working memory tasks than 9R-carrier patients. Most importantly, patients carrying a 9R allele exhibited less activation than their 10R homozygous counterparts in the prefrontal cortex, premotor cortex and caudate nucleus, when planning and executing a set-shift. This pattern was exacerbated for conditions that usually recruit the striatum compared to those that do not. This is the first study indicating that the SLC6A3/DAT1 genotype has a significant effect on fronto-striatal activation and performance in Parkinson's disease. This effect is stronger for conditions that engage the striatum. Longitudinal studies are warranted to assess this polymorphism's effect on the clinical evolution of patients with Parkinson's disease, especially with cognitive decline.</AbstractText><CopyrightInformation>© The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Habak</LastName><ForeName>Claudine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Noreau</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada 3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagano-Saito</LastName><ForeName>Atsuko</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mejía-Constaín</LastName><ForeName>Beatriz</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Degroot</LastName><ForeName>Clotilde</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Strafella</LastName><ForeName>Antonio P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>4 Movement Disorder Unit and E.J. Safra Parkinson Disease Program, Toronto Western Hospital, UHN, University of Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chouinard</LastName><ForeName>Sylvain</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lafontaine</LastName><ForeName>Anne-Louise</ForeName><Initials>AL</Initials><AffiliationInfo><Affiliation>3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rouleau</LastName><ForeName>Guy A</ForeName><Initials>GA</Initials><AffiliationInfo><Affiliation>2 Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), Montreal, Québec, Canada 3 Department of Neurology and Neurosurgery, McGill University, Montréal, QC H3A 2B4, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Monchi</LastName><ForeName>Oury</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>1 Research Centre, Institut universitaire de Gériatrie de Montréal, University of Montréal, Montréal, Québec, H3W 1W5, Canada 5 Département de Radiologie, Université de Montréal, Montréal, Québec, Canada oury.monchi@umontreal.ca.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MOP-126017</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>09</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050483">Dopamine Plasma Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493214">SLC6A3 protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Brain. 2002 Mar;125(Pt 3):584-94</RefSource><PMID Version="1">11872615</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuroimage. 2002 Jan;15(1):1-15</RefSource><PMID Version="1">11771969</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>IEEE 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MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050483" MajorTopicYN="N">Dopamine Plasma Membrane Transport Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D056344" MajorTopicYN="N">Executive Function</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005625" MajorTopicYN="N">Frontal Lobe</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059907" MajorTopicYN="N">Functional Neuroimaging</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006579" 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