Differential genetic susceptibility in diphasic and peak‐dose dyskinesias in Parkinson's disease
Identifieur interne : 001706 ( Main/Exploration ); précédent : 001705; suivant : 001707Differential genetic susceptibility in diphasic and peak‐dose dyskinesias in Parkinson's disease
Auteurs : Jee-Young Lee [Corée du Sud] ; Jinwhan Cho [Corée du Sud] ; Eun-Kyung Lee [Corée du Sud] ; Sung-Sup Park [Corée du Sud] ; Beom S. Jeon [Corée du Sud]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-01.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Antiparkinson Agents (adverse effects), Cohort Studies, D3 Dopamine receptor, Dyskinesia, Dyskinesia, Drug-Induced (classification), Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (genetics), Female, Genetic Predisposition to Disease (genetics), Genome-Wide Association Study, Genotype, Humans, Levodopa (adverse effects), Male, Middle Aged, Nervous system diseases, Parkinson Disease (drug therapy), Parkinson Disease (genetics), Parkinson disease, Parkinson's disease, Polymorphism, Genetic (genetics), Probability, Receptors, Dopamine D2 (genetics), Receptors, N-Methyl-D-Aspartate (genetics), Serotonin Plasma Membrane Transport Proteins (genetics), Young Adult, diphasic dyskinesia, dopamine receptor D3, genetic susceptibility.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- classification : Dyskinesia, Drug-Induced.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- genetics : Dyskinesia, Drug-Induced, Genetic Predisposition to Disease, Parkinson Disease, Polymorphism, Genetic, Receptors, Dopamine D2, Receptors, N-Methyl-D-Aspartate, Serotonin Plasma Membrane Transport Proteins.
- Adult, Aged, Aged, 80 and over, Cohort Studies, Female, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged, Probability, Young Adult.
Abstract
To examine whether there is a differential genetic susceptibility in the diphasic and peak‐dose forms of levodopa‐induced dyskinesias (LID) in patients with Parkinson's disease (PD). The study cohort comprised 503 unrelated Korean PD patients who were treated with levodopa and had a disease duration of at least 5 years. The presence of LID was identified during a routine follow‐up and special care was taken to separate the two distinct forms of LID into diphasic and peak‐dose dyskinesias (PDSK). Genotyping was performed in the 503 patients and in 559 healthy controls to search for polymorphisms of DRD3 p.S9G, DRD2 Taq1A, GRIN2B c.2664C>T, c.366C>G, c.‐200T>G, and the promoter region of SLC6A4. A total of 229 patients expressed LID (peak‐dose in 205, diphasic in 57, and both in 33). The presence of diphasic dyskinesia (DDSK) was exclusively associated with the DRD3 p.S9G variant after adjusting for gender, age at PD onset, Hoehn & Yahr stage, and duration of levodopa treatment. Carrying the AA genotype was likely to shorten the onset of DDSK according to the duration of levodopa therapy (P = 0.02). The presence of PDSK was not significantly associated with any of the six genetic variants studied. There may be a genetic susceptibility in the development of DDSK in PD patients on chronic levodopa therapy, and its underlying pathophysiological mechanism might be distinct from that of PDSK. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23400
Affiliations:
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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="2011-01">2011-01</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="73">73</biblScope><biblScope unit="page" to="79">79</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">1A982BA7D4C9852EBC33872847B4955255655E72</idno><idno type="DOI">10.1002/mds.23400</idno><idno type="ArticleID">MDS23400</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Antiparkinson Agents (adverse effects)</term><term>Cohort Studies</term><term>D3 Dopamine receptor</term><term>Dyskinesia</term><term>Dyskinesia, Drug-Induced (classification)</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Dyskinesia, Drug-Induced (genetics)</term><term>Female</term><term>Genetic Predisposition to Disease (genetics)</term><term>Genome-Wide Association Study</term><term>Genotype</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Male</term><term>Middle Aged</term><term>Nervous system diseases</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (genetics)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Polymorphism, Genetic (genetics)</term><term>Probability</term><term>Receptors, Dopamine D2 (genetics)</term><term>Receptors, N-Methyl-D-Aspartate (genetics)</term><term>Serotonin Plasma Membrane Transport Proteins (genetics)</term><term>Young Adult</term><term>diphasic dyskinesia</term><term>dopamine receptor D3</term><term>genetic susceptibility</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Genetic Predisposition to Disease</term><term>Parkinson Disease</term><term>Polymorphism, Genetic</term><term>Receptors, Dopamine D2</term><term>Receptors, N-Methyl-D-Aspartate</term><term>Serotonin Plasma Membrane Transport Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Cohort Studies</term><term>Female</term><term>Genome-Wide Association Study</term><term>Genotype</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Probability</term><term>Young Adult</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dyskinésie</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Récepteur dopaminergique D3</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To examine whether there is a differential genetic susceptibility in the diphasic and peak‐dose forms of levodopa‐induced dyskinesias (LID) in patients with Parkinson's disease (PD). The study cohort comprised 503 unrelated Korean PD patients who were treated with levodopa and had a disease duration of at least 5 years. The presence of LID was identified during a routine follow‐up and special care was taken to separate the two distinct forms of LID into diphasic and peak‐dose dyskinesias (PDSK). Genotyping was performed in the 503 patients and in 559 healthy controls to search for polymorphisms of DRD3 p.S9G, DRD2 Taq1A, GRIN2B c.2664C>T, c.366C>G, c.‐200T>G, and the promoter region of SLC6A4. A total of 229 patients expressed LID (peak‐dose in 205, diphasic in 57, and both in 33). The presence of diphasic dyskinesia (DDSK) was exclusively associated with the DRD3 p.S9G variant after adjusting for gender, age at PD onset, Hoehn & Yahr stage, and duration of levodopa treatment. Carrying the AA genotype was likely to shorten the onset of DDSK according to the duration of levodopa therapy (P = 0.02). The presence of PDSK was not significantly associated with any of the six genetic variants studied. There may be a genetic susceptibility in the development of DDSK in PD patients on chronic levodopa therapy, and its underlying pathophysiological mechanism might be distinct from that of PDSK. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Corée du Sud</li></country><settlement><li>Séoul</li></settlement><orgName><li>Université nationale de Séoul</li></orgName></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Lee, Jee Oung" sort="Lee, Jee Oung" uniqKey="Lee J" first="Jee-Young" last="Lee">Jee-Young Lee</name></noRegion><name sortKey="Cho, Jinwhan" sort="Cho, Jinwhan" uniqKey="Cho J" first="Jinwhan" last="Cho">Jinwhan Cho</name><name sortKey="Jeon, Beom S" sort="Jeon, Beom S" uniqKey="Jeon B" first="Beom S." last="Jeon">Beom S. Jeon</name><name sortKey="Jeon, Beom S" sort="Jeon, Beom S" uniqKey="Jeon B" first="Beom S." last="Jeon">Beom S. Jeon</name><name sortKey="Jeon, Beom S" sort="Jeon, Beom S" uniqKey="Jeon B" first="Beom S." last="Jeon">Beom S. Jeon</name><name sortKey="Lee, Eun Yung" sort="Lee, Eun Yung" uniqKey="Lee E" first="Eun-Kyung" last="Lee">Eun-Kyung Lee</name><name sortKey="Lee, Eun Yung" sort="Lee, Eun Yung" uniqKey="Lee E" first="Eun-Kyung" last="Lee">Eun-Kyung Lee</name><name sortKey="Park, Sung Up" sort="Park, Sung Up" uniqKey="Park S" first="Sung-Sup" last="Park">Sung-Sup Park</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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