Plasma α‐synuclein in patients with Parkinson's disease with and without treatment
Identifieur interne : 001B02 ( Main/Curation ); précédent : 001B01; suivant : 001B03Plasma α‐synuclein in patients with Parkinson's disease with and without treatment
Auteurs : Raquel Duran [Espagne] ; Francisco J. Barrero [Espagne] ; Blas Morales [Espagne] ; Juan D. Luna [Espagne] ; Manuel Ramirez [Espagne] ; Francisco Vives [Espagne]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-03-15.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (therapeutic use), Drug Therapy (statistics & numerical data), Enzyme-Linked Immunosorbent Assay, Female, Human, Humans, Levodopa (therapeutic use), Male, Middle Aged, Nervous system diseases, Parkinson Disease (blood), Parkinson Disease (drug therapy), Parkinson Disease (epidemiology), Parkinson disease, Parkinson's disease, Parkinson's disease treatment, Treatment, alpha-Synuclein (blood), pathogenesis, plasma, α‐synuclein.
- MESH :
- chemical , blood : alpha-Synuclein.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- blood : Parkinson Disease.
- drug therapy : Parkinson Disease.
- epidemiology : Parkinson Disease.
- statistics & numerical data : Drug Therapy.
- Aged, Enzyme-Linked Immunosorbent Assay, Female, Humans, Male, Middle Aged.
Abstract
Alpha‐synuclein (α‐syn) is an intracellular protein with a high tendency to aggregation. It is the major component of Lewy bodies and may play a key role in the pathogenesis of Parkinson's disease (PD). α‐Syn is also released by neurons and can be detected in biological fluids, such as plasma. The purpose of this study was to determine whether plasma α‐syn concentrations are elevated in newly diagnosed PD patients before treatment (nontreated PD group, ntPD; n = 53) and to compare them with concentrations in PD patients with at least 1 year of specific treatment (tPD; n = 42) and in healthy controls (n = 60). Plasma α‐syn concentrations in the ntPD and tPD groups were similar and significantly higher than in healthy controls. In conclusion, α‐syn was elevated early in the development of PD and specific PD treatment did not change plasma α‐syn levels. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22928
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<front><div type="abstract" xml:lang="en">Alpha‐synuclein (α‐syn) is an intracellular protein with a high tendency to aggregation. It is the major component of Lewy bodies and may play a key role in the pathogenesis of Parkinson's disease (PD). α‐Syn is also released by neurons and can be detected in biological fluids, such as plasma. The purpose of this study was to determine whether plasma α‐syn concentrations are elevated in newly diagnosed PD patients before treatment (nontreated PD group, ntPD; n = 53) and to compare them with concentrations in PD patients with at least 1 year of specific treatment (tPD; n = 42) and in healthy controls (n = 60). Plasma α‐syn concentrations in the ntPD and tPD groups were similar and significantly higher than in healthy controls. In conclusion, α‐syn was elevated early in the development of PD and specific PD treatment did not change plasma α‐syn levels. © 2010 Movement Disorder Society</div>
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<front><div type="abstract" xml:lang="en">Alpha-synuclein (α-syn) is an intracellular protein with a high tendency to aggregation. It is the major component of Lewy bodies and may play a key role in the pathogenesis of Parkinson's disease (PD). α-Syn is also released by neurons and can be detected in biological fluids, such as plasma. The purpose of this study was to determine whether plasma α-syn concentrations are elevated in newly diagnosed PD patients before treatment (nontreated PD group, ntPD; n = 53) and to compare them with concentrations in PD patients with at least 1 year of specific treatment (tPD; n = 42) and in healthy controls (n = 60). Plasma α-syn concentrations in the ntPD and tPD groups were similar and significantly higher than in healthy controls. In conclusion, α-syn was elevated early in the development of PD and specific PD treatment did not change plasma α-syn levels.</div>
</front>
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<author><name sortKey="Duran, Raquel" sort="Duran, Raquel" uniqKey="Duran R" first="Raquel" last="Duran">Raquel Duran</name>
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<author><name sortKey="Barrero, Francisco J" sort="Barrero, Francisco J" uniqKey="Barrero F" first="Francisco J." last="Barrero">Francisco J. Barrero</name>
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<author><name sortKey="Morales, Blas" sort="Morales, Blas" uniqKey="Morales B" first="Blas" last="Morales">Blas Morales</name>
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<author><name sortKey="Luna, Juan D" sort="Luna, Juan D" uniqKey="Luna J" first="Juan D." last="Luna">Juan D. Luna</name>
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<author><name sortKey="Ramirez, Manuel" sort="Ramirez, Manuel" uniqKey="Ramirez M" first="Manuel" last="Ramirez">Manuel Ramirez</name>
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<author><name sortKey="Vives, Francisco" sort="Vives, Francisco" uniqKey="Vives F" first="Francisco" last="Vives">Francisco Vives</name>
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<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Plasma α‐synuclein in patients with Parkinson's disease with and without treatment</title>
<author><name sortKey="Duran, Raquel" sort="Duran, Raquel" uniqKey="Duran R" first="Raquel" last="Duran">Raquel Duran</name>
<affiliation wicri:level="4"><country xml:lang="fr">Espagne</country>
<wicri:regionArea>Department of Physiology and Institute of Neurosciences, Centro de Investigaciones Biomedicas (CIBM), University of Granada, Granada</wicri:regionArea>
<orgName type="university">Université de Grenade</orgName>
<placeName><settlement type="city">Grenade (Espagne)</settlement>
<region nuts="2" type="region">Andalousie</region>
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<author><name sortKey="Barrero, Francisco J" sort="Barrero, Francisco J" uniqKey="Barrero F" first="Francisco J." last="Barrero">Francisco J. Barrero</name>
<affiliation wicri:level="1"><country xml:lang="fr">Espagne</country>
<wicri:regionArea>Movement Disorder Unit, Department of Neurology, San Cecilio University Hospital, Granada</wicri:regionArea>
<wicri:noRegion>Granada</wicri:noRegion>
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<author><name sortKey="Morales, Blas" sort="Morales, Blas" uniqKey="Morales B" first="Blas" last="Morales">Blas Morales</name>
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<wicri:regionArea>Movement Disorder Unit, Department of Neurology, San Cecilio University Hospital, Granada</wicri:regionArea>
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<author><name sortKey="Luna, Juan D" sort="Luna, Juan D" uniqKey="Luna J" first="Juan D." last="Luna">Juan D. Luna</name>
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<wicri:regionArea>Department of Statistics, Faculty of Medicine, University of Granada</wicri:regionArea>
<placeName><settlement type="city">Grenade (Espagne)</settlement>
<region nuts="2" type="region">Andalousie</region>
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<orgName type="university">Université de Grenade</orgName>
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<author><name sortKey="Ramirez, Manuel" sort="Ramirez, Manuel" uniqKey="Ramirez M" first="Manuel" last="Ramirez">Manuel Ramirez</name>
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<wicri:regionArea>Unit of Physiology, Department of Health Sciences, University of Jaén, Jaén</wicri:regionArea>
<wicri:noRegion>Jaén</wicri:noRegion>
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<author><name sortKey="Vives, Francisco" sort="Vives, Francisco" uniqKey="Vives F" first="Francisco" last="Vives">Francisco Vives</name>
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<wicri:regionArea>Department of Physiology and Institute of Neurosciences, Centro de Investigaciones Biomedicas (CIBM), University of Granada, Granada</wicri:regionArea>
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<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>
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<pubPlace>Hoboken</pubPlace>
<date type="published" when="2010-03-15">2010-03-15</date>
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<term>Antiparkinson Agents (therapeutic use)</term>
<term>Drug Therapy (statistics & numerical data)</term>
<term>Enzyme-Linked Immunosorbent Assay</term>
<term>Female</term>
<term>Humans</term>
<term>Levodopa (therapeutic use)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Parkinson Disease (blood)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (epidemiology)</term>
<term>Parkinson's disease</term>
<term>Parkinson's disease treatment</term>
<term>alpha-Synuclein (blood)</term>
<term>pathogenesis</term>
<term>plasma</term>
<term>α‐synuclein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>alpha-Synuclein</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="statistics & numerical data" xml:lang="en"><term>Drug Therapy</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Enzyme-Linked Immunosorbent Assay</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
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<front><div type="abstract" xml:lang="en">Alpha‐synuclein (α‐syn) is an intracellular protein with a high tendency to aggregation. It is the major component of Lewy bodies and may play a key role in the pathogenesis of Parkinson's disease (PD). α‐Syn is also released by neurons and can be detected in biological fluids, such as plasma. The purpose of this study was to determine whether plasma α‐syn concentrations are elevated in newly diagnosed PD patients before treatment (nontreated PD group, ntPD; n = 53) and to compare them with concentrations in PD patients with at least 1 year of specific treatment (tPD; n = 42) and in healthy controls (n = 60). Plasma α‐syn concentrations in the ntPD and tPD groups were similar and significantly higher than in healthy controls. In conclusion, α‐syn was elevated early in the development of PD and specific PD treatment did not change plasma α‐syn levels. © 2010 Movement Disorder Society</div>
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