Experimental models of Parkinson's disease: from the static to the dynamic.
Identifieur interne : 001493 ( PubMed/Corpus ); précédent : 001492; suivant : 001494Experimental models of Parkinson's disease: from the static to the dynamic.
Auteurs : E. Bezard ; C. Imbert ; C E GrossSource :
- Reviews in the neurosciences [ 0334-1763 ] ; 1998.
English descriptors
- KwdEn :
- MESH :
- classification : Parkinson Disease.
- pathology : Parkinson Disease.
- physiopathology : Parkinson Disease.
- Animals, Disease Models, Animal.
Abstract
The experimental models of Parkinson's disease (PD) available today can be divided into two categories according to the mode of action of the compound used: transient pharmacological impairment of dopaminergic transmission along the nigrostriatal pathway or selective destruction by a neurotoxic agent of the dopaminergic neurons of the substantia nigra pars compacta. The present article looks at the relative merits of each model, the clinical symptoms and neuronal impairment it induces, and the contribution it could make to the development of a truly dynamic model. It is becoming more and more clear that there is an urgent need for a chronic model integrating all the clinical features of PD including resting tremor, and reproducing the gradual but continuous nigral degeneration observed in the human pathology. Discrepancies have been reported several times between results obtained in classic animal models and those described in PD, and it would seem probable that such contradictions can be ascribed to the fact that animal models do not, as yet, reproduce the continuous evolution of the human disease. Dynamic experimental models which come closer to the progressive neurodegeneration and gradual intensification of motor disability so characteristic of human PD will enable us to investigate crucial aspects of the disease, such as compensatory mechanisms and dyskinesia.
PubMed: 9711900
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pubmed:9711900Le document en format XML
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Imbert</name></author><author><name sortKey="Gross, C E" sort="Gross, C E" uniqKey="Gross C" first="C E" last="Gross">C E Gross</name></author></analytic><series><title level="j">Reviews in the neurosciences</title><idno type="ISSN">0334-1763</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Parkinson Disease (classification)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The experimental models of Parkinson's disease (PD) available today can be divided into two categories according to the mode of action of the compound used: transient pharmacological impairment of dopaminergic transmission along the nigrostriatal pathway or selective destruction by a neurotoxic agent of the dopaminergic neurons of the substantia nigra pars compacta. The present article looks at the relative merits of each model, the clinical symptoms and neuronal impairment it induces, and the contribution it could make to the development of a truly dynamic model. It is becoming more and more clear that there is an urgent need for a chronic model integrating all the clinical features of PD including resting tremor, and reproducing the gradual but continuous nigral degeneration observed in the human pathology. Discrepancies have been reported several times between results obtained in classic animal models and those described in PD, and it would seem probable that such contradictions can be ascribed to the fact that animal models do not, as yet, reproduce the continuous evolution of the human disease. Dynamic experimental models which come closer to the progressive neurodegeneration and gradual intensification of motor disability so characteristic of human PD will enable us to investigate crucial aspects of the disease, such as compensatory mechanisms and dyskinesia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">9711900</PMID><DateCreated><Year>1999</Year><Month>05</Month><Day>21</Day></DateCreated><DateCompleted><Year>1999</Year><Month>05</Month><Day>21</Day></DateCompleted><DateRevised><Year>2006</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0334-1763</ISSN><JournalIssue CitedMedium="Print"><Volume>9</Volume><Issue>2</Issue><PubDate><Year>1998</Year></PubDate></JournalIssue><Title>Reviews in the neurosciences</Title><ISOAbbreviation>Rev Neurosci</ISOAbbreviation></Journal><ArticleTitle>Experimental models of Parkinson's disease: from the static to the dynamic.</ArticleTitle><Pagination><MedlinePgn>71-90</MedlinePgn></Pagination><Abstract><AbstractText>The experimental models of Parkinson's disease (PD) available today can be divided into two categories according to the mode of action of the compound used: transient pharmacological impairment of dopaminergic transmission along the nigrostriatal pathway or selective destruction by a neurotoxic agent of the dopaminergic neurons of the substantia nigra pars compacta. The present article looks at the relative merits of each model, the clinical symptoms and neuronal impairment it induces, and the contribution it could make to the development of a truly dynamic model. It is becoming more and more clear that there is an urgent need for a chronic model integrating all the clinical features of PD including resting tremor, and reproducing the gradual but continuous nigral degeneration observed in the human pathology. Discrepancies have been reported several times between results obtained in classic animal models and those described in PD, and it would seem probable that such contradictions can be ascribed to the fact that animal models do not, as yet, reproduce the continuous evolution of the human disease. 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