Multitracer assessment of dopamine function after transplantation of embryonic stem cell‐derived neural stem cells in a primate model of Parkinson's disease
Identifieur interne : 001E75 ( Main/Curation ); précédent : 001E74; suivant : 001E76Multitracer assessment of dopamine function after transplantation of embryonic stem cell‐derived neural stem cells in a primate model of Parkinson's disease
Auteurs : Shin-Ichi Muramatsu [Japon] ; Tsuyoshi Okuno [Japon] ; Yutaka Suzuki [Japon] ; Takashi Nakayama [Japon] ; Takeharu Kakiuchi [Japon] ; Naomi Takino [Japon] ; Asako Iida [Japon] ; Fumiko Ono [Japon] ; Keiji Terao [Japon] ; Nobuo Inoue [Japon] ; Imaharu Nakano [Japon] ; Yasushi Kondo [Japon] ; Hideo Tsukada [Japon]Source :
- Synapse [ 0887-4476 ] ; 2009-07.
English descriptors
Abstract
The ability of primate embryonic stem (ES) cells to differentiate into dopamine (DA)‐synthesizing neurons has raised hopes of creating novel cell therapies for Parkinson's disease (PD). As the primary purpose of cell transplantation in PD is restoration of dopaminergic neurotransmission in the striatum, in vivo assessment of DA function after grafting is necessary to achieve better therapeutic effects. A chronic model of PD was produced in two cynomolgus monkeys (M‐1 and M‐2) by systemic administration of neurotoxin. Neural stem cells (NSCs) derived from cynomolgus ES cells were implanted unilaterally in the putamen. To evaluate DA‐specific functions, we used multiple [11C]‐labeled positron emission tomography (PET) tracers, including [β‐11C]L‐3,4‐dihydroxyphenylalanine (L‐[β‐11C]DOPA, DA precursor ligand), [11C]‐2β‐carbomethoxy‐3β‐(4‐fluorophenyl)tropane ([11C]β‐CFT, DA transporter ligand) and [11C]raclopride (D2 receptor ligand). At 12 weeks after grafting NSCs, PET demonstrated significantly increased uptake of L‐[β‐11C]DOPA (M‐1:41%, M‐2:61%) and [11C]β‐CFT (M‐1:31%, M‐2:36%) uptake in the grafted putamen. In addition, methamphetamine challenge in M‐2 induced reduced [11C]raclopride binding (16%) in the transplanted putamen, suggesting release of DA. These results show that transplantation of NSCs derived from cynomolgus monkey ES cells can restore DA function in the putamen of a primate model of PD. PET with multitracers is useful for functional studies in developing cell‐based therapies against PD. Synapse 63: 541‐548, 2009. © 2009 Wiley‐Liss, Inc.
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DOI: 10.1002/syn.20634
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disease</title><author><name sortKey="Muramatsu, Shin Chi" sort="Muramatsu, Shin Chi" uniqKey="Muramatsu S" first="Shin-Ichi" last="Muramatsu">Shin-Ichi Muramatsu</name><affiliation wicri:level="1"><mods:affiliation>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498</wicri:regionArea></affiliation></author><author><name sortKey="Okuno, Tsuyoshi" sort="Okuno, Tsuyoshi" uniqKey="Okuno T" first="Tsuyoshi" last="Okuno">Tsuyoshi Okuno</name><affiliation wicri:level="1"><mods:affiliation>Mitsubishi Tanabe Pharma Corporation, Osaka 532‐8505, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Mitsubishi Tanabe Pharma Corporation, Osaka 532‐8505</wicri:regionArea></affiliation></author><author><name sortKey="Suzuki, Yutaka" sort="Suzuki, Yutaka" uniqKey="Suzuki 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wicri:level="1"><mods:affiliation>Central Research Laboratory, Hamamatsu Photonics K.K., Shizuoka 434‐8601, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Central Research Laboratory, Hamamatsu Photonics K.K., Shizuoka 434‐8601</wicri:regionArea></affiliation></author><author><name sortKey="Takino, Naomi" sort="Takino, Naomi" uniqKey="Takino N" first="Naomi" last="Takino">Naomi Takino</name><affiliation wicri:level="1"><mods:affiliation>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498</wicri:regionArea></affiliation></author><author><name sortKey="Iida, Asako" sort="Iida, Asako" uniqKey="Iida A" first="Asako" last="Iida">Asako Iida</name><affiliation wicri:level="1"><mods:affiliation>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498</wicri:regionArea></affiliation></author><author><name sortKey="Ono, Fumiko" sort="Ono, Fumiko" uniqKey="Ono F" first="Fumiko" last="Ono">Fumiko Ono</name><affiliation wicri:level="1"><mods:affiliation>Tsukuba Primate Research Center, National Institute of Biomedical Innovation, Ibaraki 305‐0843, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Tsukuba Primate Research Center, National Institute of Biomedical Innovation, Ibaraki 305‐0843</wicri:regionArea></affiliation></author><author><name sortKey="Terao, Keiji" sort="Terao, Keiji" uniqKey="Terao K" first="Keiji" last="Terao">Keiji Terao</name><affiliation wicri:level="1"><mods:affiliation>Tsukuba Primate Research Center, National Institute of Biomedical Innovation, Ibaraki 305‐0843, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Tsukuba Primate Research Center, National Institute of Biomedical Innovation, Ibaraki 305‐0843</wicri:regionArea></affiliation></author><author><name sortKey="Inoue, Nobuo" sort="Inoue, Nobuo" uniqKey="Inoue N" first="Nobuo" last="Inoue">Nobuo Inoue</name><affiliation wicri:level="1"><mods:affiliation>Division of Regenerative Neurosciences, Tokyo Metropolitan University, Tokyo 116‐8551, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Regenerative Neurosciences, Tokyo Metropolitan University, Tokyo 116‐8551</wicri:regionArea></affiliation></author><author><name sortKey="Nakano, Imaharu" sort="Nakano, Imaharu" uniqKey="Nakano I" first="Imaharu" last="Nakano">Imaharu Nakano</name><affiliation wicri:level="1"><mods:affiliation>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Divison of Neurology, Department of Medicine, Jichi Medical University, Tochigi 329‐0498</wicri:regionArea></affiliation></author><author><name sortKey="Kondo, Yasushi" sort="Kondo, Yasushi" uniqKey="Kondo Y" first="Yasushi" last="Kondo">Yasushi Kondo</name><affiliation wicri:level="1"><mods:affiliation>Mitsubishi Tanabe Pharma Corporation, Osaka 532‐8505, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Mitsubishi Tanabe Pharma Corporation, Osaka 532‐8505</wicri:regionArea></affiliation></author><author><name sortKey="Tsukada, Hideo" sort="Tsukada, Hideo" uniqKey="Tsukada H" first="Hideo" last="Tsukada">Hideo Tsukada</name><affiliation wicri:level="1"><mods:affiliation>Central Research Laboratory, Hamamatsu Photonics K.K., Shizuoka 434‐8601, Japan</mods:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Central Research Laboratory, Hamamatsu Photonics K.K., Shizuoka 434‐8601</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Synapse</title><title level="j" type="abbrev">Synapse</title><idno type="ISSN">0887-4476</idno><idno type="eISSN">1098-2396</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009-07">2009-07</date><biblScope unit="volume">63</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="541">541</biblScope><biblScope unit="page" to="548">548</biblScope></imprint><idno type="ISSN">0887-4476</idno></series><idno type="istex">493F050D7EAA94FFA13E53E2530CA3D2352717FA</idno><idno type="DOI">10.1002/syn.20634</idno><idno type="ArticleID">SYN20634</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0887-4476</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>ES cell</term><term>MPTP</term><term>PET</term><term>monkey</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The ability of primate embryonic stem (ES) cells to differentiate into dopamine (DA)‐synthesizing neurons has raised hopes of creating novel cell therapies for Parkinson's disease (PD). As the primary purpose of cell transplantation in PD is restoration of dopaminergic neurotransmission in the striatum, in vivo assessment of DA function after grafting is necessary to achieve better therapeutic effects. A chronic model of PD was produced in two cynomolgus monkeys (M‐1 and M‐2) by systemic administration of neurotoxin. Neural stem cells (NSCs) derived from cynomolgus ES cells were implanted unilaterally in the putamen. To evaluate DA‐specific functions, we used multiple [11C]‐labeled positron emission tomography (PET) tracers, including [β‐11C]L‐3,4‐dihydroxyphenylalanine (L‐[β‐11C]DOPA, DA precursor ligand), [11C]‐2β‐carbomethoxy‐3β‐(4‐fluorophenyl)tropane ([11C]β‐CFT, DA transporter ligand) and [11C]raclopride (D2 receptor ligand). At 12 weeks after grafting NSCs, PET demonstrated significantly increased uptake of L‐[β‐11C]DOPA (M‐1:41%, M‐2:61%) and [11C]β‐CFT (M‐1:31%, M‐2:36%) uptake in the grafted putamen. In addition, methamphetamine challenge in M‐2 induced reduced [11C]raclopride binding (16%) in the transplanted putamen, suggesting release of DA. These results show that transplantation of NSCs derived from cynomolgus monkey ES cells can restore DA function in the putamen of a primate model of PD. PET with multitracers is useful for functional studies in developing cell‐based therapies against PD. Synapse 63: 541‐548, 2009. © 2009 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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