Rotigotine treatment partially protects from MPTP toxicity in a progressive macaque model of Parkinson's disease
Clinical DA agonist monotherapy trials, which used in vivo imaging of the DA transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical da...
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| Veröffentlicht in: | Experimental neurology Jg. 203; H. 2; S. 415 - 422 |
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| Sprache: | Englisch |
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01.02.2007
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| ISSN: | 0014-4886 |
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| Abstract | Clinical DA agonist monotherapy trials, which used in vivo imaging of the DA transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical data by testing the protective property of the continuously delivered D3/D2/D1 dopamine receptor agonist rotigotine. Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned (MPTP) macaque model that mimics the progression of Parkinson's disease in vivo ([99mTc]-TRODAT-1 single photon emission computed tomography (SPECT)) and ex vivo ([125I]-nortropane DAT labelling) endpoints were evaluated. After 38 days of treatment followed by two weeks of washout, rotigotine-treated animals were significantly less parkinsonian than the vehicle-treated ones. Such behavioural difference is the consequence of a partial protection of the DA terminals as could be confirmed by ex vivo DAT labelling. However, the protection of nerve terminals was not detected using SPECT. The data suggest that rotigotine exerts partial protection but that conventional imaging would not be able to identify such protection. |
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| AbstractList | Clinical DA agonist monotherapy trials, which used in vivo imaging of the DA transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical data by testing the protective property of the continuously delivered D3/D2/D1 dopamine receptor agonist rotigotine. Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned (MPTP) macaque model that mimics the progression of Parkinson's disease in vivo ([99mTc]-TRODAT-1 single photon emission computed tomography (SPECT)) and ex vivo ([125I]-nortropane DAT labelling) endpoints were evaluated. After 38 days of treatment followed by two weeks of washout, rotigotine-treated animals were significantly less parkinsonian than the vehicle-treated ones. Such behavioural difference is the consequence of a partial protection of the DA terminals as could be confirmed by ex vivo DAT labelling. However, the protection of nerve terminals was not detected using SPECT. The data suggest that rotigotine exerts partial protection but that conventional imaging would not be able to identify such protection.Clinical DA agonist monotherapy trials, which used in vivo imaging of the DA transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical data by testing the protective property of the continuously delivered D3/D2/D1 dopamine receptor agonist rotigotine. Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned (MPTP) macaque model that mimics the progression of Parkinson's disease in vivo ([99mTc]-TRODAT-1 single photon emission computed tomography (SPECT)) and ex vivo ([125I]-nortropane DAT labelling) endpoints were evaluated. After 38 days of treatment followed by two weeks of washout, rotigotine-treated animals were significantly less parkinsonian than the vehicle-treated ones. Such behavioural difference is the consequence of a partial protection of the DA terminals as could be confirmed by ex vivo DAT labelling. However, the protection of nerve terminals was not detected using SPECT. The data suggest that rotigotine exerts partial protection but that conventional imaging would not be able to identify such protection. Clinical DA agonist monotherapy trials, which used in vivo imaging of the DA transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical data by testing the protective property of the continuously delivered D3/D2/D1 dopamine receptor agonist rotigotine. Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned (MPTP) macaque model that mimics the progression of Parkinson's disease in vivo ([99mTc]-TRODAT-1 single photon emission computed tomography (SPECT)) and ex vivo ([125I]-nortropane DAT labelling) endpoints were evaluated. After 38 days of treatment followed by two weeks of washout, rotigotine-treated animals were significantly less parkinsonian than the vehicle-treated ones. Such behavioural difference is the consequence of a partial protection of the DA terminals as could be confirmed by ex vivo DAT labelling. However, the protection of nerve terminals was not detected using SPECT. The data suggest that rotigotine exerts partial protection but that conventional imaging would not be able to identify such protection. Clinical da agonist monotherapy trials, which used in vivo imaging of the da transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical data by testing the protective property of the continuously delivered D sub(3)/D sub(2)/D sub(1) dopamine receptor agonist rotigotine. Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned (MPTP) macaque model that mimics the progression of Parkinson's disease in vivo ([ super(99m)Tc]-TRODAT-1 single photon emission computed tomography (SPECT)) and ex vivo ([ super(125)I]-nortropane DAT labelling) endpoints were evaluated. After 38 days of treatment followed by two weeks of washout, rotigotine- treated animals were significantly less parkinsonian than the vehicle-treated ones. Such behavioural difference is the consequence of a partial protection of the da terminals as could be confirmed by ex vivo DAT labelling. However, the protection of nerve terminals was not detected using SPECT. The data suggest that rotigotine exerts partial protection but that conventional imaging would not be able to identify such protection. Clinical DA agonist monotherapy trials, which used in vivo imaging of the DA transporter (DAT) to assess the rate of progression of nigrostriatal degeneration, have failed to demonstrate consistent evidence for neuroprotection. The present study aims at reconciling these experimental and clinical data by testing the protective property of the continuously delivered D3/D2/D1 dopamine receptor agonist rotigotine. Using a progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned (MPTP) macaque model that mimics the progression of Parkinson's disease in vivo ([99mTc]-TRODAT-1 single photon emission computed tomography (SPECT)) and ex vivo ([125I]-nortropane DAT labelling) endpoints were evaluated. After 38 days of treatment followed by two weeks of washout, rotigotine-treated animals were significantly less parkinsonian than the vehicle-treated ones. Such behavioural difference is the consequence of a partial protection of the DA terminals as could be confirmed by ex vivo DAT labelling. However, the protection of nerve terminals was not detected using SPECT. The data suggest that rotigotine exerts partial protection but that conventional imaging would not be able to identify such protection. |
| Author | Crossman, Alan R. Wu, Tao Guigoni, Celine Scheller, Dieter Ravenscroft, Paula Hill, Michael Chan, Piu Li, Qin Zhang, Renling Bezard, Erwan Guan, Le |
| Author_xml | – sequence: 1 givenname: Dieter surname: Scheller fullname: Scheller, Dieter email: dieter.scheller@schwarzpharma.com organization: SCHWARZ BIOSCIENCES GmbH, Alfred-Nobel Strasse 10, Monheim, Germany – sequence: 2 givenname: Piu surname: Chan fullname: Chan, Piu organization: Department of Neurology, Xuanwu Hospital, Beijing, Peoples Republic of China – sequence: 3 givenname: Qin surname: Li fullname: Li, Qin organization: Motac Neuroscience Ltd., Manchester, UK – sequence: 4 givenname: Tao surname: Wu fullname: Wu, Tao organization: Department of Neurology, Xuanwu Hospital, Beijing, Peoples Republic of China – sequence: 5 givenname: Renling surname: Zhang fullname: Zhang, Renling organization: Department of Nuclear Medicine, Xuanwu Hospital, Beijing, Peoples Republic of China – sequence: 6 givenname: Le surname: Guan fullname: Guan, Le organization: Department of Nuclear Medicine, Xuanwu Hospital, Beijing, Peoples Republic of China – sequence: 7 givenname: Paula surname: Ravenscroft fullname: Ravenscroft, Paula organization: Motac Neuroscience Ltd., Manchester, UK – sequence: 8 givenname: Celine surname: Guigoni fullname: Guigoni, Celine organization: CNRS UMR 5543, Université Victor Segalen, Bordeaux, France – sequence: 9 givenname: Alan R. surname: Crossman fullname: Crossman, Alan R. organization: Motac Neuroscience Ltd., Manchester, UK – sequence: 10 givenname: Michael surname: Hill fullname: Hill, Michael organization: Motac Neuroscience Ltd., Manchester, UK – sequence: 11 givenname: Erwan surname: Bezard fullname: Bezard, Erwan organization: CNRS UMR 5543, Université Victor Segalen, Bordeaux, France |
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| Keywords | ST SNc ROI SPECT [125I]-nortropane Striatum [99mTc]-TRODAT Autoradiography PD TH DAT Dopamine agonist l-DOPA Dopamine transporter MPTP Substantia nigra pars compacta DA PET CB Toxicity Central nervous system Monkey Parkinson disease D3 Dopamine receptor Prevention Ex vivo Primates Rotigotine Clinical trial Degenerative disease Degeneration Nervous system diseases Experimental data Dopamine Mimic D1 Dopamine receptor Single photon emission tomography Catecholamine Experimental study Photon Cerebral disorder Vertebrata Mammalia Locus niger D2 Dopamine receptor Treatment Animal Central nervous system disease Neurotransmitter Models Extrapyramidal syndrome |
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| Title | Rotigotine treatment partially protects from MPTP toxicity in a progressive macaque model of Parkinson's disease |
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