High dose levodopa therapy is not toxic in multiple system atrophy: Experimental evidence
Identifieur interne : 002E17 ( Main/Exploration ); précédent : 002E16; suivant : 002E18High dose levodopa therapy is not toxic in multiple system atrophy: Experimental evidence
Auteurs : Nadia Stefanova [Autriche] ; Martin Köllensperger [Autriche] ; Monika Hainzer [Autriche] ; Angela Cenci [Suède] ; Werner Poewe [Autriche] ; Gregor Karl Wenning [Autriche]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-05-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Analysis of Variance, Animal, Animal Diseases, Animals, Antiparkinson Agents (therapeutic use), Corpus Striatum (drug effects), Corpus Striatum (metabolism), Dose-Response Relationship, Drug, High dose, Inclusion, Levodopa, Levodopa (therapeutic use), Mice, Mice, Inbred C57BL, Mice, Transgenic, Motor Activity (drug effects), Motor Activity (physiology), Mouse, Multiple System Atrophy (drug therapy), Multiple System Atrophy (genetics), Multiple System Atrophy (physiopathology), Multiple system atrophy, Nerve Tissue Proteins (metabolism), Nervous system diseases, Treatment, alpha-Synuclein (genetics), alpha-Synuclein (metabolism), glial cytoplasmic inclusions, levodopa, multiple system atrophy, neurodegeneration, transgenic mouse, α‐synuclein.
- MESH :
- chemical , genetics : alpha-Synuclein.
- chemical , metabolism : Nerve Tissue Proteins, alpha-Synuclein.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug effects : Corpus Striatum, Motor Activity.
- drug therapy : Multiple System Atrophy.
- genetics : Multiple System Atrophy.
- metabolism : Corpus Striatum.
- physiology : Motor Activity.
- physiopathology : Multiple System Atrophy.
- Analysis of Variance, Animal Diseases, Animals, Dose-Response Relationship, Drug, Mice, Mice, Inbred C57BL, Mice, Transgenic.
Abstract
Levodopa is generally regarded the first choice therapy for parkinsonism associated with multiple system atrophy (MSA‐P). However, MSA‐P patients often show a poor or unsustained levodopa response which inflicts high dose therapy. This is generally attributed to progressive striatal degeneration with loss of dopamine receptors. Experimental evidence suggests that dopaminergic stimulation may accelerate the striatal disease process in MSA, possibly by pro‐oxidative mechanisms. Intact nigrostriatal dopamine release augments striatal lesion size in the unilateral nigral and striatal double lesion rat model of MSA‐P. Further, neuronal vulnerability to exogenous oxidative stress is increased in a transgenic MSA mouse model with oligodendroglial α‐synuclein inclusions. The aim of the present study was to analyze whether high dose levodopa delivery in the transgenic MSA model is associated with neurotoxicity exacerbated by the presence of oligodendroglial α‐synuclein inclusion pathology. Control and transgenic MSA mice underwent pulsatile treatment with either vehicle, low or high dose levodopa for a period of 1 month. Behavioral and neuropathological indices failed to show evidence for neurotoxic effects of high‐dose levodopa in this α‐synuclein transgenic MSA model. These findings support the idea that high dose levodopa therapy in MSA is not detrimental to the underlying neuropathological process. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21468
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="2007-05-15">2007-05-15</date><biblScope unit="vol">22</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="969">969</biblScope><biblScope unit="page" to="973">973</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">6B7E5055AFC3F5038582E4B2CC952A3F1EFE4D2C</idno><idno type="DOI">10.1002/mds.21468</idno><idno type="ArticleID">MDS21468</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Animal</term><term>Animal Diseases</term><term>Animals</term><term>Antiparkinson Agents (therapeutic use)</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (metabolism)</term><term>Dose-Response Relationship, Drug</term><term>High dose</term><term>Inclusion</term><term>Levodopa</term><term>Levodopa (therapeutic use)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Motor Activity (drug effects)</term><term>Motor Activity (physiology)</term><term>Mouse</term><term>Multiple System Atrophy (drug therapy)</term><term>Multiple System Atrophy (genetics)</term><term>Multiple System Atrophy (physiopathology)</term><term>Multiple system atrophy</term><term>Nerve Tissue Proteins (metabolism)</term><term>Nervous system diseases</term><term>Treatment</term><term>alpha-Synuclein (genetics)</term><term>alpha-Synuclein (metabolism)</term><term>glial cytoplasmic inclusions</term><term>levodopa</term><term>multiple system atrophy</term><term>neurodegeneration</term><term>transgenic mouse</term><term>α‐synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nerve Tissue Proteins</term><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="drug effects" xml:lang="en"><term>Corpus Striatum</term><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animal Diseases</term><term>Animals</term><term>Dose-Response Relationship, Drug</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Animal</term><term>Atrophie multisystématisée</term><term>Dose forte</term><term>Inclusion</term><term>Lévodopa</term><term>Souris</term><term>Système nerveux pathologie</term><term>Traitement</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Levodopa is generally regarded the first choice therapy for parkinsonism associated with multiple system atrophy (MSA‐P). However, MSA‐P patients often show a poor or unsustained levodopa response which inflicts high dose therapy. This is generally attributed to progressive striatal degeneration with loss of dopamine receptors. Experimental evidence suggests that dopaminergic stimulation may accelerate the striatal disease process in MSA, possibly by pro‐oxidative mechanisms. Intact nigrostriatal dopamine release augments striatal lesion size in the unilateral nigral and striatal double lesion rat model of MSA‐P. Further, neuronal vulnerability to exogenous oxidative stress is increased in a transgenic MSA mouse model with oligodendroglial α‐synuclein inclusions. The aim of the present study was to analyze whether high dose levodopa delivery in the transgenic MSA model is associated with neurotoxicity exacerbated by the presence of oligodendroglial α‐synuclein inclusion pathology. Control and transgenic MSA mice underwent pulsatile treatment with either vehicle, low or high dose levodopa for a period of 1 month. Behavioral and neuropathological indices failed to show evidence for neurotoxic effects of high‐dose levodopa in this α‐synuclein transgenic MSA model. These findings support the idea that high dose levodopa therapy in MSA is not detrimental to the underlying neuropathological process. © 2007 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Autriche</li><li>Suède</li></country><region><li>Tyrol (Land)</li></region><settlement><li>Innsbruck</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><country name="Autriche"><noRegion><name sortKey="Stefanova, Nadia" sort="Stefanova, Nadia" uniqKey="Stefanova N" first="Nadia" last="Stefanova">Nadia Stefanova</name></noRegion><name sortKey="Hainzer, Monika" sort="Hainzer, Monika" uniqKey="Hainzer M" first="Monika" last="Hainzer">Monika Hainzer</name><name sortKey="Kollensperger, Martin" sort="Kollensperger, Martin" uniqKey="Kollensperger M" first="Martin" last="Köllensperger">Martin Köllensperger</name><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><name sortKey="Wenning, Gregor Karl" sort="Wenning, Gregor Karl" uniqKey="Wenning G" first="Gregor Karl" last="Wenning">Gregor Karl Wenning</name></country><country name="Suède"><noRegion><name sortKey="Cenci, Angela" sort="Cenci, Angela" uniqKey="Cenci A" first="Angela" last="Cenci">Angela Cenci</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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