Microglial activation and dopamine terminal loss in early Parkinson's disease
Identifieur interne : 001467 ( Main/Exploration ); précédent : 001466; suivant : 001468Microglial activation and dopamine terminal loss in early Parkinson's disease
Auteurs : Yasuomi Ouchi ; Etsuji Yoshikawa [Japon] ; Yoshimoto Sekine [Japon] ; Masami Futatsubashi [Japon] ; Toshihiko Kanno ; Tomomi Ogusu [Japon] ; Tatsuo TorizukaSource :
- Annals of Neurology [ 0364-5134 ] ; 2005-02.
Abstract
Neuroinflammatory glial response may contribute to degenerative processes in Parkinson's disease (PD). To investigate changes in microglial activity associated with changes in the presynaptic dopamine transporter density in the PD brain in vivo, we studied 10 early‐stage drug‐naive PD patients twice using positron emission tomography with a radiotracer for activated microglia [11C](R)‐PK11195 and a dopamine transporter marker [11C]CFT. Quantitative levels of binding potentials (BPs) of [11C](R)‐PK11195 and [11C]CFT in the nigrostriatal pathway were estimated by compartment analyses. The levels of [11C](R)‐PK11195 BP in the midbrain contralateral to the clinically affected side were significantly higher in PD than that in 10 age‐matched healthy subjects. The midbrain [11C](R)‐PK11195 BP levels significantly correlated inversely with [11C]CFT BP in the putamen and correlated positively with the motor severity assessed by the Unified Parkinson's Disease Rating Scale in PD. In healthy subjects, the [11C](R)‐PK11195 BP in the thalamus and midbrain showed an age‐dependent increase. In vivo demonstration of parallel changes in microglial activation and corresponding dopaminergic terminal loss in the affected nigrostriatal pathway in early PD supports that neuroinflammatory responses by intrinsic microglia contribute significantly to the progressive degeneration process of the disease and suggests the importance of early therapeutic intervention with neuroprotective drugs. Ann Neurol 2005;57:168–175
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DOI: 10.1002/ana.20338
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uniqKey="Ogusu T" first="Tomomi" last="Ogusu">Tomomi Ogusu</name></author><author><name sortKey="Torizuka, Tatsuo" sort="Torizuka, Tatsuo" uniqKey="Torizuka T" first="Tatsuo" last="Torizuka">Tatsuo Torizuka</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9E34285E75D5749165F19A792BC8259B4BDC2CFF</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1002/ana.20338</idno><idno type="url">https://api.istex.fr/document/9E34285E75D5749165F19A792BC8259B4BDC2CFF/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001574</idno><idno type="wicri:Area/Main/Curation">001343</idno><idno type="wicri:Area/Main/Exploration">001467</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Microglial activation and dopamine terminal loss in early Parkinson's disease</title><author><name sortKey="Ouchi, Yasuomi" sort="Ouchi, Yasuomi" uniqKey="Ouchi Y" first="Yasuomi" last="Ouchi">Yasuomi 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sortKey="Futatsubashi, Masami" sort="Futatsubashi, Masami" uniqKey="Futatsubashi M" first="Masami" last="Futatsubashi">Masami Futatsubashi</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Central Research Laboratory, Hamamatsu Photonics K.K., Hamakita</wicri:regionArea><wicri:noRegion>Hamakita</wicri:noRegion></affiliation></author><author><name sortKey="Kanno, Toshihiko" sort="Kanno, Toshihiko" uniqKey="Kanno T" first="Toshihiko" last="Kanno">Toshihiko Kanno</name><affiliation><wicri:noCountry code="subField">Hamamatsu Medical Center</wicri:noCountry></affiliation></author><author><name sortKey="Ogusu, Tomomi" sort="Ogusu, Tomomi" uniqKey="Ogusu T" first="Tomomi" last="Ogusu">Tomomi Ogusu</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>Central Research Laboratory, Hamamatsu Photonics K.K., Hamakita</wicri:regionArea><wicri:noRegion>Hamakita</wicri:noRegion></affiliation></author><author><name sortKey="Torizuka, Tatsuo" sort="Torizuka, Tatsuo" uniqKey="Torizuka T" first="Tatsuo" last="Torizuka">Tatsuo Torizuka</name><affiliation><wicri:noCountry code="subField">Hamamatsu Medical Center</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-02">2005-02</date><biblScope unit="volume">57</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="168">168</biblScope><biblScope unit="page" to="175">175</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">9E34285E75D5749165F19A792BC8259B4BDC2CFF</idno><idno type="DOI">10.1002/ana.20338</idno><idno type="ArticleID">ANA20338</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neuroinflammatory glial response may contribute to degenerative processes in Parkinson's disease (PD). To investigate changes in microglial activity associated with changes in the presynaptic dopamine transporter density in the PD brain in vivo, we studied 10 early‐stage drug‐naive PD patients twice using positron emission tomography with a radiotracer for activated microglia [11C](R)‐PK11195 and a dopamine transporter marker [11C]CFT. Quantitative levels of binding potentials (BPs) of [11C](R)‐PK11195 and [11C]CFT in the nigrostriatal pathway were estimated by compartment analyses. The levels of [11C](R)‐PK11195 BP in the midbrain contralateral to the clinically affected side were significantly higher in PD than that in 10 age‐matched healthy subjects. The midbrain [11C](R)‐PK11195 BP levels significantly correlated inversely with [11C]CFT BP in the putamen and correlated positively with the motor severity assessed by the Unified Parkinson's Disease Rating Scale in PD. In healthy subjects, the [11C](R)‐PK11195 BP in the thalamus and midbrain showed an age‐dependent increase. In vivo demonstration of parallel changes in microglial activation and corresponding dopaminergic terminal loss in the affected nigrostriatal pathway in early PD supports that neuroinflammatory responses by intrinsic microglia contribute significantly to the progressive degeneration process of the disease and suggests the importance of early therapeutic intervention with neuroprotective drugs. Ann Neurol 2005;57:168–175</div></front></TEI><affiliations><list><country><li>Japon</li></country></list><tree><noCountry><name sortKey="Kanno, Toshihiko" sort="Kanno, Toshihiko" uniqKey="Kanno T" first="Toshihiko" last="Kanno">Toshihiko Kanno</name><name sortKey="Ouchi, Yasuomi" sort="Ouchi, Yasuomi" uniqKey="Ouchi Y" first="Yasuomi" last="Ouchi">Yasuomi Ouchi</name><name sortKey="Torizuka, Tatsuo" sort="Torizuka, Tatsuo" uniqKey="Torizuka T" first="Tatsuo" last="Torizuka">Tatsuo Torizuka</name></noCountry><country name="Japon"><noRegion><name sortKey="Yoshikawa, Etsuji" sort="Yoshikawa, Etsuji" uniqKey="Yoshikawa E" first="Etsuji" last="Yoshikawa">Etsuji Yoshikawa</name></noRegion><name sortKey="Futatsubashi, Masami" sort="Futatsubashi, Masami" uniqKey="Futatsubashi M" first="Masami" last="Futatsubashi">Masami Futatsubashi</name><name sortKey="Ogusu, Tomomi" sort="Ogusu, Tomomi" uniqKey="Ogusu T" first="Tomomi" last="Ogusu">Tomomi Ogusu</name><name sortKey="Sekine, Yoshimoto" sort="Sekine, Yoshimoto" uniqKey="Sekine Y" first="Yoshimoto" last="Sekine">Yoshimoto Sekine</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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