Catechol‐O‐methyltransferase val158met and cognitive function in Parkinson's disease
Identifieur interne : 001E11 ( Main/Exploration ); précédent : 001E10; suivant : 001E12Catechol‐O‐methyltransferase val158met and cognitive function in Parkinson's disease
Auteurs : Jeroen Hoogland [Pays-Bas] ; Rob M. A. De Bie [Pays-Bas] ; Caroline H. Williams-Gray [Royaume-Uni] ; Dino Muslimovi [Pays-Bas] ; Ben Schmand [Pays-Bas] ; Bart Post [Pays-Bas]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Age Factors, Aged, Analysis of Variance, Attention (physiology), Catechol O-Methyltransferase (genetics), Catechol O-methyltransferase, Cognition (physiology), Cognition Disorders (genetics), Cognition Disorders (physiopathology), Cognition Disorders (psychology), Cognitive disorder, Executive Function (physiology), Executive function, Female, Genotype, Humans, Male, Middle Aged, Nervous system diseases, Neuropsychological Tests, Parkinson Disease (genetics), Parkinson Disease (physiopathology), Parkinson Disease (psychology), Parkinson disease, Parkinson's disease, Polymorphism, Single Nucleotide, Sex Factors, catechol‐O‐methyltransferase, cognitive deficits, executive function.
- MESH :
- chemical , genetics : Catechol O-Methyltransferase.
- genetics : Cognition Disorders, Parkinson Disease.
- physiology : Attention, Cognition, Executive Function.
- physiopathology : Cognition Disorders, Parkinson Disease.
- psychology : Cognition Disorders, Parkinson Disease.
- Age Factors, Aged, Analysis of Variance, Female, Genotype, Humans, Male, Middle Aged, Neuropsychological Tests, Polymorphism, Single Nucleotide, Sex Factors.
Abstract
Cognitive dysfunction is one of the most incapacitating non‐motor symptoms of Parkinson's disease (PD). Some cognitive deficits are thought to be related to abnormal dopamine homeostasis. The latter is influenced by catechol‐O‐methyltransferase (COMT), an enzyme that degrades dopamine. Previous research suggests a relationship between the COMT val158met functional polymorphism (SNP) and measures of executive function. We evaluated this hypothesis in a cohort of PD patients with an extensive neuropsychological test battery. Cognitive assessment and COMT genotyping were performed in 153 early PD patients from outpatient clinics general hospitals in the Netherlands. Our results do not support a direct effect of COMT val158met genotype on performance on neuropsychological measures of attention and executive function, but they suggest that genotype may interact with dopaminergic medication use to influence cognitive ability. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23319
Affiliations:
- Pays-Bas, Royaume-Uni
- Angleterre, Angleterre de l'Est, Gueldre, Hollande-Septentrionale
- Amsterdam, Cambridge, Nimègue
- Université de Cambridge
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Le document en format XML
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Williams-Gray</name><affiliation wicri:level="4"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, Cambridge Centre for Brain Repair, University of Cambridge</wicri:regionArea><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName><orgName type="university">Université de Cambridge</orgName></affiliation></author><author><name sortKey="Muslimovi, Dino" sort="Muslimovi, Dino" uniqKey="Muslimovi D" first="Dino" last="Muslimovi">Dino Muslimovi</name><affiliation wicri:level="3"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam</wicri:regionArea><placeName><settlement type="city">Amsterdam</settlement><region nuts="2" type="province">Hollande-Septentrionale</region></placeName></affiliation></author><author><name sortKey="Schmand, Ben" sort="Schmand, Ben" uniqKey="Schmand B" first="Ben" last="Schmand">Ben Schmand</name><affiliation wicri:level="3"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam</wicri:regionArea><placeName><settlement type="city">Amsterdam</settlement><region nuts="2" type="province">Hollande-Septentrionale</region></placeName></affiliation></author><author><name sortKey="Post, Bart" sort="Post, Bart" uniqKey="Post B" first="Bart" last="Post">Bart Post</name><affiliation wicri:level="3"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam</wicri:regionArea><placeName><settlement type="city">Amsterdam</settlement><region nuts="2" type="province">Hollande-Septentrionale</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, UMCN St. Radboud, Nijmegen</wicri:regionArea><placeName><settlement type="city">Nimègue</settlement><region type="province" nuts="2">Gueldre</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-11-15">2010-11-15</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2550">2550</biblScope><biblScope unit="page" to="2554">2554</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3223DABC00D61528A60996811F37E1095525EAF5</idno><idno type="DOI">10.1002/mds.23319</idno><idno type="ArticleID">MDS23319</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors</term><term>Aged</term><term>Analysis of Variance</term><term>Attention (physiology)</term><term>Catechol O-Methyltransferase (genetics)</term><term>Catechol O-methyltransferase</term><term>Cognition (physiology)</term><term>Cognition Disorders (genetics)</term><term>Cognition Disorders (physiopathology)</term><term>Cognition Disorders (psychology)</term><term>Cognitive disorder</term><term>Executive Function (physiology)</term><term>Executive function</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Nervous system diseases</term><term>Neuropsychological Tests</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (psychology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Polymorphism, Single Nucleotide</term><term>Sex Factors</term><term>catechol‐O‐methyltransferase</term><term>cognitive deficits</term><term>executive function</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Catechol O-Methyltransferase</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cognition Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Attention</term><term>Cognition</term><term>Executive Function</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cognition Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Cognition Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Aged</term><term>Analysis of Variance</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Polymorphism, Single Nucleotide</term><term>Sex Factors</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Catechol O-methyltransferase</term><term>Fonction exécutive</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Trouble cognitif</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cognitive dysfunction is one of the most incapacitating non‐motor symptoms of Parkinson's disease (PD). Some cognitive deficits are thought to be related to abnormal dopamine homeostasis. The latter is influenced by catechol‐O‐methyltransferase (COMT), an enzyme that degrades dopamine. Previous research suggests a relationship between the COMT val158met functional polymorphism (SNP) and measures of executive function. We evaluated this hypothesis in a cohort of PD patients with an extensive neuropsychological test battery. Cognitive assessment and COMT genotyping were performed in 153 early PD patients from outpatient clinics general hospitals in the Netherlands. Our results do not support a direct effect of COMT val158met genotype on performance on neuropsychological measures of attention and executive function, but they suggest that genotype may interact with dopaminergic medication use to influence cognitive ability. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Pays-Bas</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Angleterre de l'Est</li><li>Gueldre</li><li>Hollande-Septentrionale</li></region><settlement><li>Amsterdam</li><li>Cambridge</li><li>Nimègue</li></settlement><orgName><li>Université de Cambridge</li></orgName></list><tree><country name="Pays-Bas"><region name="Hollande-Septentrionale"><name sortKey="Hoogland, Jeroen" sort="Hoogland, Jeroen" uniqKey="Hoogland J" first="Jeroen" last="Hoogland">Jeroen Hoogland</name></region><name sortKey="De Bie, Rob M A" sort="De Bie, Rob M A" uniqKey="De Bie R" first="Rob M. A." last="De Bie">Rob M. A. De Bie</name><name sortKey="Muslimovi, Dino" sort="Muslimovi, Dino" uniqKey="Muslimovi D" first="Dino" last="Muslimovi">Dino Muslimovi</name><name sortKey="Post, Bart" sort="Post, Bart" uniqKey="Post B" first="Bart" last="Post">Bart Post</name><name sortKey="Post, Bart" sort="Post, Bart" uniqKey="Post B" first="Bart" last="Post">Bart Post</name><name sortKey="Schmand, Ben" sort="Schmand, Ben" uniqKey="Schmand B" first="Ben" last="Schmand">Ben Schmand</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Williams Ray, Caroline H" sort="Williams Ray, Caroline H" uniqKey="Williams Ray C" first="Caroline H." last="Williams-Gray">Caroline H. Williams-Gray</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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