Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue
Identifieur interne : 000F12 ( Istex/Corpus ); précédent : 000F11; suivant : 000F13Transplantation in Parkinson's disease: PET changes correlate with the amount of grafted tissue
Auteurs : Valérie Cochen ; Maria-Joao Ribeiro ; Jean-Paul Nguyen ; Jean-Marc Gurruchaga ; Gabriel Villafane ; Christian Loc'H ; Gilles Defer ; Yves Samson ; Marc Peschanski ; Philippe Hantraye ; Pierre Cesaro ; Philippe RemySource :
- Movement Disorders [ 0885-3185 ] ; 2003-08.
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- KwdEn :
Abstract
An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;12:119). We compared the striatal uptake of [18F]fluorodopa with [76Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [18F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10463
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<front><div type="abstract" xml:lang="en">An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;12:119). We compared the striatal uptake of [18F]fluorodopa with [76Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [18F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society</div>
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<p>We compared the striatal uptake of [<sup>18</sup>
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<abstract lang="en">An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;12:119). We compared the striatal uptake of [18F]fluorodopa with [76Br]‐FE‐CBT, a positron emission tomography (PET) ligand of the dopamine transporter (DAT), which estimates the density of dopamine nerve terminals, in 6 patients with Parkinson's disease grafted with fetal mesencephalic cells. There was no change in DAT ligand binding in the grafted putamen, despite a significant increase of [18F]fluorodopa uptake. This finding suggests that the clinical benefit induced by the graft is more related to increased dopaminergic activity than improved dopaminergic innervation in the host striatum and, therefore, that [18F]fluorodopa remains the optimal tracer to evaluate grafted PD patients. Further analysis showed that the clinical and [18F]fluorodopa uptake changes after the grafts were correlated with the number of ventral mesencephalae used for implantation. © 2003 Movement Disorder Society</abstract>
<note type="funding">Ministère de la Santé - No. PHRC‐96138; </note>
<note type="funding">Fondation pour la Recherche Médicale</note>
<subject lang="en"><genre>Keywords</genre>
<topic>Parkinson</topic>
<topic>fetal transplantation</topic>
<topic>PET</topic>
<topic>dopamine transporter</topic>
<topic>CIT</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated"><title>Mov. Disord.</title>
</titleInfo>
<subject><genre>article category</genre>
<topic>Brief Report</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part><date>2003</date>
<detail type="volume"><caption>vol.</caption>
<number>18</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>8</number>
</detail>
<extent unit="pages"><start>928</start>
<end>932</end>
<total>6</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">27F23CAAF90303E367C943AB008DA5282B9F509F</identifier>
<identifier type="DOI">10.1002/mds.10463</identifier>
<identifier type="ArticleID">MDS10463</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Movement Disorder Society</accessCondition>
<recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
</recordInfo>
</mods>
</metadata>
<serie></serie>
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