A double‐blind, placebo‐controlled study to assess the mitochondria‐targeted antioxidant MitoQ as a disease‐modifying therapy in Parkinson's disease
Identifieur interne : 002326 ( Main/Merge ); précédent : 002325; suivant : 002327A double‐blind, placebo‐controlled study to assess the mitochondria‐targeted antioxidant MitoQ as a disease‐modifying therapy in Parkinson's disease
Auteurs : Barry J. Snow [Nouvelle-Zélande] ; Fiona L. Rolfe [Nouvelle-Zélande] ; Michelle M. Lockhart [Nouvelle-Zélande] ; Christopher M. Frampton [Nouvelle-Zélande] ; John D. O'Sullivan [Australie] ; Victor Fung [Australie] ; Robin A. J. Smith [Nouvelle-Zélande] ; Michael P. Murphy [Royaume-Uni] ; Kenneth M. Taylor [Nouvelle-Zélande]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-08-15.
English descriptors
- KwdEn :
- Adult, Aged, Antioxidants (therapeutic use), Dose-Response Relationship, Drug, Double-Blind Method, Female, Humans, Male, Middle Aged, MitoQ, Organophosphorus Compounds (therapeutic use), PD, Parkinson Disease (drug therapy), Time Factors, Treatment Outcome, Ubiquinone (analogs & derivatives), Ubiquinone (therapeutic use), mitochondria, neuroprotection, oxidative damage.
- MESH :
- chemical , analogs & derivatives : Ubiquinone.
- chemical , therapeutic use : Antioxidants, Organophosphorus Compounds, Ubiquinone.
- drug therapy : Parkinson Disease.
- Adult, Aged, Dose-Response Relationship, Drug, Double-Blind Method, Female, Humans, Male, Middle Aged, Time Factors, Treatment Outcome.
Abstract
Multiple lines of evidence point to mitochondrial oxidative stress as a potential pathogenic cause for Parkinson's disease (PD). MitoQ is a powerful mitochondrial antioxidant. It is absorbed orally and concentrates within mitochondria where it has been shown to protect against oxidative damage. We enrolled 128 newly diagnosed untreated patients with PD in a double‐blind study of two doses of MitoQ compared with placebo to explore the hypothesis that, over 12 months, MitoQ would slow the progression of PD as measured by clinical scores, particularly the Unified Parkinson Disease Rating Scale. We showed no difference between MitoQ and placebo on any measure of PD progression. MitoQ does not slow the progression of PD, and this finding should be taken into account when considering the oxidative stress hypothesis for the pathogenesis of PD. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23148
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<front><div type="abstract" xml:lang="en">Multiple lines of evidence point to mitochondrial oxidative stress as a potential pathogenic cause for Parkinson's disease (PD). MitoQ is a powerful mitochondrial antioxidant. It is absorbed orally and concentrates within mitochondria where it has been shown to protect against oxidative damage. We enrolled 128 newly diagnosed untreated patients with PD in a double‐blind study of two doses of MitoQ compared with placebo to explore the hypothesis that, over 12 months, MitoQ would slow the progression of PD as measured by clinical scores, particularly the Unified Parkinson Disease Rating Scale. We showed no difference between MitoQ and placebo on any measure of PD progression. MitoQ does not slow the progression of PD, and this finding should be taken into account when considering the oxidative stress hypothesis for the pathogenesis of PD. © 2010 Movement Disorder Society</div>
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<front><div type="abstract" xml:lang="en">Multiple lines of evidence point to mitochondrial oxidative stress as a potential pathogenic cause for Parkinson's disease (PD). MitoQ is a powerful mitochondrial antioxidant. It is absorbed orally and concentrates within mitochondria where it has been shown to protect against oxidative damage. We enrolled 128 newly diagnosed untreated patients with PD in a double‐blind study of two doses of MitoQ compared with placebo to explore the hypothesis that, over 12 months, MitoQ would slow the progression of PD as measured by clinical scores, particularly the Unified Parkinson Disease Rating Scale. We showed no difference between MitoQ and placebo on any measure of PD progression. MitoQ does not slow the progression of PD, and this finding should be taken into account when considering the oxidative stress hypothesis for the pathogenesis of PD. © 2010 Movement Disorder Society</div>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">A double-blind, placebo-controlled study to assess the mitochondria-targeted antioxidant MitoQ as a disease-modifying therapy in Parkinson's disease.</title>
<author><name sortKey="Snow, Barry J" sort="Snow, Barry J" uniqKey="Snow B" first="Barry J" last="Snow">Barry J. Snow</name>
<affiliation wicri:level="1"><nlm:affiliation>Neurology Department, Auckland Hospital, Auckland, New Zealand. bsnow@adhb.govt.nz</nlm:affiliation>
<country xml:lang="fr">Nouvelle-Zélande</country>
<wicri:regionArea>Neurology Department, Auckland Hospital, Auckland</wicri:regionArea>
<wicri:noRegion>Auckland</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Rolfe, Fiona L" sort="Rolfe, Fiona L" uniqKey="Rolfe F" first="Fiona L" last="Rolfe">Fiona L. Rolfe</name>
</author>
<author><name sortKey="Lockhart, Michelle M" sort="Lockhart, Michelle M" uniqKey="Lockhart M" first="Michelle M" last="Lockhart">Michelle M. Lockhart</name>
</author>
<author><name sortKey="Frampton, Christopher M" sort="Frampton, Christopher M" uniqKey="Frampton C" first="Christopher M" last="Frampton">Christopher M. Frampton</name>
</author>
<author><name sortKey="O Sullivan, John D" sort="O Sullivan, John D" uniqKey="O Sullivan J" first="John D" last="O'Sullivan">John D. O'Sullivan</name>
</author>
<author><name sortKey="Fung, Victor" sort="Fung, Victor" uniqKey="Fung V" first="Victor" last="Fung">Victor Fung</name>
</author>
<author><name sortKey="Smith, Robin A J" sort="Smith, Robin A J" uniqKey="Smith R" first="Robin A J" last="Smith">Robin A J. Smith</name>
</author>
<author><name sortKey="Murphy, Michael P" sort="Murphy, Michael P" uniqKey="Murphy M" first="Michael P" last="Murphy">Michael P. Murphy</name>
</author>
<author><name sortKey="Taylor, Kenneth M" sort="Taylor, Kenneth M" uniqKey="Taylor K" first="Kenneth M" last="Taylor">Kenneth M. Taylor</name>
</author>
</analytic>
<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="eISSN">1531-8257</idno>
<imprint><date when="2010" type="published">2010</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Antioxidants (therapeutic use)</term>
<term>Dose-Response Relationship, Drug</term>
<term>Double-Blind Method</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Organophosphorus Compounds (therapeutic use)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Time Factors</term>
<term>Treatment Outcome</term>
<term>Ubiquinone (analogs & derivatives)</term>
<term>Ubiquinone (therapeutic use)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Ubiquinone</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antioxidants</term>
<term>Organophosphorus Compounds</term>
<term>Ubiquinone</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Dose-Response Relationship, Drug</term>
<term>Double-Blind Method</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Time Factors</term>
<term>Treatment Outcome</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Multiple lines of evidence point to mitochondrial oxidative stress as a potential pathogenic cause for Parkinson's disease (PD). MitoQ is a powerful mitochondrial antioxidant. It is absorbed orally and concentrates within mitochondria where it has been shown to protect against oxidative damage. We enrolled 128 newly diagnosed untreated patients with PD in a double-blind study of two doses of MitoQ compared with placebo to explore the hypothesis that, over 12 months, MitoQ would slow the progression of PD as measured by clinical scores, particularly the Unified Parkinson Disease Rating Scale. We showed no difference between MitoQ and placebo on any measure of PD progression. MitoQ does not slow the progression of PD, and this finding should be taken into account when considering the oxidative stress hypothesis for the pathogenesis of PD.</div>
</front>
</TEI>
</PubMed>
</double>
</record>
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