Intrastriatal injection of an adenoviral vector expressing glial-cell-line-derived neurotrophic factor prevents dopaminergic neuron degeneration and behavioral impairment in a rat model of Parkinson disease.
Identifieur interne : 001396 ( PubMed/Checkpoint ); précédent : 001395; suivant : 001397Intrastriatal injection of an adenoviral vector expressing glial-cell-line-derived neurotrophic factor prevents dopaminergic neuron degeneration and behavioral impairment in a rat model of Parkinson disease.
Auteurs : A. Bilang-Bleuel [France] ; F. Revah ; P. Colin ; I. Locquet ; J J Robert ; J. Mallet ; P. HorellouSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 1997.
English descriptors
- KwdEn :
- Adenoviridae, Animals, Behavior, Animal (drug effects), Disease Models, Animal, Female, Gene Transfer Techniques, Genetic Therapy, Genetic Vectors, Glial Cell Line-Derived Neurotrophic Factor, Nerve Growth Factors, Nerve Tissue Proteins (administration & dosage), Nerve Tissue Proteins (genetics), Neurons (drug effects), Neurons (pathology), Neuroprotective Agents (administration & dosage), Parkinson Disease (drug therapy), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (pathology), Rats, Rats, Sprague-Dawley.
- MESH :
- chemical , administration & dosage : Nerve Tissue Proteins, Neuroprotective Agents.
- chemical , genetics : Nerve Tissue Proteins.
- chemical : Glial Cell Line-Derived Neurotrophic Factor, Nerve Growth Factors.
- drug effects : Behavior, Animal, Neurons.
- drug therapy : Parkinson Disease.
- genetics : Parkinson Disease.
- metabolism : Parkinson Disease.
- pathology : Neurons, Parkinson Disease.
- Adenoviridae, Animals, Disease Models, Animal, Female, Gene Transfer Techniques, Genetic Therapy, Genetic Vectors, Rats, Rats, Sprague-Dawley.
Abstract
Glial-cell-line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for adult nigral dopamine neurons in vivo. GDNF has both protective and restorative effects on the nigro-striatal dopaminergic (DA) system in animal models of Parkinson disease. Appropriate administration of this factor is essential for the success of its clinical application. Since it cannot cross the blood-brain barrier, a gene transfer method may be appropriate for delivery of the trophic factor to DA cells. We have constructed a recombinant adenovirus (Ad) encoding GDNF and injected it into rat striatum to make use of its ability to infect neurons and to be retrogradely transported by DA neurons. Ad-GDNF was found to drive production of large amounts of GDNF, as quantified by ELISA. The GDNF produced after gene transfer was biologically active: it increased the survival and differentiation of DA neurons in vitro. To test the efficacy of the Ad-mediated GDNF gene transfer in vivo, we used a progressive lesion model of Parkinson disease. Rats received injections unilaterally into their striatum first of Ad and then 6 days later of 6-hydroxydopamine. We found that mesencephalic nigral dopamine neurons of animals treated with the Ad-GDNF were protected, whereas those of animals treated with the Ad-beta-galactosidase were not. This protection was associated with a difference in motor function: amphetamine-induced turning was much lower in animals that received the Ad-GDNF than in the animals that received Ad-beta-galactosidase. This finding may have implications for the development of a treatment for Parkinson disease based on the use of neurotrophic factors.
PubMed: 9238061
Affiliations:
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pubmed:9238061Le document en format XML
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<front><div type="abstract" xml:lang="en">Glial-cell-line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for adult nigral dopamine neurons in vivo. GDNF has both protective and restorative effects on the nigro-striatal dopaminergic (DA) system in animal models of Parkinson disease. Appropriate administration of this factor is essential for the success of its clinical application. Since it cannot cross the blood-brain barrier, a gene transfer method may be appropriate for delivery of the trophic factor to DA cells. We have constructed a recombinant adenovirus (Ad) encoding GDNF and injected it into rat striatum to make use of its ability to infect neurons and to be retrogradely transported by DA neurons. Ad-GDNF was found to drive production of large amounts of GDNF, as quantified by ELISA. The GDNF produced after gene transfer was biologically active: it increased the survival and differentiation of DA neurons in vitro. To test the efficacy of the Ad-mediated GDNF gene transfer in vivo, we used a progressive lesion model of Parkinson disease. Rats received injections unilaterally into their striatum first of Ad and then 6 days later of 6-hydroxydopamine. We found that mesencephalic nigral dopamine neurons of animals treated with the Ad-GDNF were protected, whereas those of animals treated with the Ad-beta-galactosidase were not. This protection was associated with a difference in motor function: amphetamine-induced turning was much lower in animals that received the Ad-GDNF than in the animals that received Ad-beta-galactosidase. This finding may have implications for the development of a treatment for Parkinson disease based on the use of neurotrophic factors.</div>
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<Abstract><AbstractText>Glial-cell-line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for adult nigral dopamine neurons in vivo. GDNF has both protective and restorative effects on the nigro-striatal dopaminergic (DA) system in animal models of Parkinson disease. Appropriate administration of this factor is essential for the success of its clinical application. Since it cannot cross the blood-brain barrier, a gene transfer method may be appropriate for delivery of the trophic factor to DA cells. We have constructed a recombinant adenovirus (Ad) encoding GDNF and injected it into rat striatum to make use of its ability to infect neurons and to be retrogradely transported by DA neurons. Ad-GDNF was found to drive production of large amounts of GDNF, as quantified by ELISA. The GDNF produced after gene transfer was biologically active: it increased the survival and differentiation of DA neurons in vitro. To test the efficacy of the Ad-mediated GDNF gene transfer in vivo, we used a progressive lesion model of Parkinson disease. Rats received injections unilaterally into their striatum first of Ad and then 6 days later of 6-hydroxydopamine. We found that mesencephalic nigral dopamine neurons of animals treated with the Ad-GDNF were protected, whereas those of animals treated with the Ad-beta-galactosidase were not. This protection was associated with a difference in motor function: amphetamine-induced turning was much lower in animals that received the Ad-GDNF than in the animals that received Ad-beta-galactosidase. This finding may have implications for the development of a treatment for Parkinson disease based on the use of neurotrophic factors.</AbstractText>
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<name sortKey="Robert, J J" sort="Robert, J J" uniqKey="Robert J" first="J J" last="Robert">J J Robert</name>
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<country name="France"><region name="Île-de-France"><name sortKey="Bilang Bleuel, A" sort="Bilang Bleuel, A" uniqKey="Bilang Bleuel A" first="A" last="Bilang-Bleuel">A. Bilang-Bleuel</name>
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