Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man
Identifieur interne : 002209 ( Main/Exploration ); précédent : 002208; suivant : 002210Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man
Auteurs : M. Gerlach [Allemagne] ; P. Riederer [Allemagne]Source :
- Journal of Neural Transmission [ 0300-9564 ] ; 1996-08-01.
Abstract
Summary: Animal models are an important aid in experimental medical science because they enable one to study the pathogenetic mechanisms and the therapeutic principles of treating the functional disturbances (symptoms) of human diseases. Once the causative mechanism is understood, animal models are also helpful in the development of therapeutic approaches exploiting this understanding. On the basis of experimental and clinical findings. Parkinson's disease (PD) became the first neurological disease to be treated palliatively by neurotransmitter replacement therapy. The pathological hallmark of PD is a specific degeneration of nigral and other pigmented brainstem nuclei, with a characteristic inclusion, the Lewy body, in remaining nerve cells. There is now a lot of evidence that degeneration of the dopaminergic nigral neurones and the resulting striatal dopamine-deficiency syndrome are responsible for its classic motor symptoms akinesia and bradykinesia. PD is one of many human diseases which do not appear to have spontaneously arisen in animals. The characteristic features of the disease can however be more or less faithfully imitated in animals through the administration of various neurotoxic agents and drugs disturbing the dopaminergic neurotransmission. The cause of chronic nigral cell death in PD and the underlying mechanisms remain elusive. The partial elucidation of the processes underlie the selective action of neurotoxic substances such as 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has however revealed possible molecular mechanisms that give rise to neuronal death. Accordingly, hypotheses concerning the mechanisms of these neurotoxines have been related to the pathogenesis of nigral cell death in PD. The present contribution starts out by describing some of the clinical, pathological and neurochemical phenomena of PD. The currently most important animal models (e.g. the reserpine model, neuroleptic-induced catalepsy, tremor models, experimentally-induced degeneration of nigro-striatal dopaminergic neurons with 6-OHDA, methamphetamine, MPTP, MPP+, tetrahydroisoquinolines, β-carbolines, and iron) critically reviewed next, and are compared with the characteristic features of the disease in man.
Url:
DOI: 10.1007/BF01291788
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man</title>
<author><name sortKey="Gerlach, M" sort="Gerlach, M" uniqKey="Gerlach M" first="M." last="Gerlach">M. Gerlach</name>
</author>
<author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:64788B7E5263D0789468923A04FC1C66D18CF971</idno>
<date when="1996" year="1996">1996</date>
<idno type="doi">10.1007/BF01291788</idno>
<idno type="url">https://api.istex.fr/document/64788B7E5263D0789468923A04FC1C66D18CF971/fulltext/pdf</idno>
<idno type="wicri:Area/Main/Corpus">000E32</idno>
<idno type="wicri:Area/Main/Curation">000C65</idno>
<idno type="wicri:Area/Main/Exploration">002209</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man</title>
<author><name sortKey="Gerlach, M" sort="Gerlach, M" uniqKey="Gerlach M" first="M." last="Gerlach">M. Gerlach</name>
<affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Clinical Neurochemistry, University Neurological Clinic, University of Würzburg</wicri:regionArea>
<wicri:noRegion>University of Würzburg</wicri:noRegion>
<wicri:noRegion>University of Würzburg</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Clinical Neurochemistry, University Neurological Clinic, St. Josef's Hospital, Bochum</wicri:regionArea>
<wicri:noRegion>Bochum</wicri:noRegion>
<wicri:noRegion>Bochum</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name>
<affiliation wicri:level="1"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Clinical Neurochemistry, University Neurological Clinic, University of Würzburg</wicri:regionArea>
<wicri:noRegion>University of Würzburg</wicri:noRegion>
<wicri:noRegion>University of Würzburg</wicri:noRegion>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Journal of Neural Transmission</title>
<title level="j" type="sub">Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</title>
<title level="j" type="abbrev">J. Neural Transmission</title>
<idno type="ISSN">0300-9564</idno>
<idno type="eISSN">1435-1463</idno>
<imprint><publisher>Springer-Verlag</publisher>
<pubPlace>Vienna</pubPlace>
<date type="published" when="1996-08-01">1996-08-01</date>
<biblScope unit="volume">103</biblScope>
<biblScope unit="issue">8-9</biblScope>
<biblScope unit="page" from="987">987</biblScope>
<biblScope unit="page" to="1041">1041</biblScope>
</imprint>
<idno type="ISSN">0300-9564</idno>
</series>
<idno type="istex">64788B7E5263D0789468923A04FC1C66D18CF971</idno>
<idno type="DOI">10.1007/BF01291788</idno>
<idno type="ArticleID">Art9</idno>
<idno type="ArticleID">BF01291788</idno>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0300-9564</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass></textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Summary: Animal models are an important aid in experimental medical science because they enable one to study the pathogenetic mechanisms and the therapeutic principles of treating the functional disturbances (symptoms) of human diseases. Once the causative mechanism is understood, animal models are also helpful in the development of therapeutic approaches exploiting this understanding. On the basis of experimental and clinical findings. Parkinson's disease (PD) became the first neurological disease to be treated palliatively by neurotransmitter replacement therapy. The pathological hallmark of PD is a specific degeneration of nigral and other pigmented brainstem nuclei, with a characteristic inclusion, the Lewy body, in remaining nerve cells. There is now a lot of evidence that degeneration of the dopaminergic nigral neurones and the resulting striatal dopamine-deficiency syndrome are responsible for its classic motor symptoms akinesia and bradykinesia. PD is one of many human diseases which do not appear to have spontaneously arisen in animals. The characteristic features of the disease can however be more or less faithfully imitated in animals through the administration of various neurotoxic agents and drugs disturbing the dopaminergic neurotransmission. The cause of chronic nigral cell death in PD and the underlying mechanisms remain elusive. The partial elucidation of the processes underlie the selective action of neurotoxic substances such as 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has however revealed possible molecular mechanisms that give rise to neuronal death. Accordingly, hypotheses concerning the mechanisms of these neurotoxines have been related to the pathogenesis of nigral cell death in PD. The present contribution starts out by describing some of the clinical, pathological and neurochemical phenomena of PD. The currently most important animal models (e.g. the reserpine model, neuroleptic-induced catalepsy, tremor models, experimentally-induced degeneration of nigro-striatal dopaminergic neurons with 6-OHDA, methamphetamine, MPTP, MPP+, tetrahydroisoquinolines, β-carbolines, and iron) critically reviewed next, and are compared with the characteristic features of the disease in man.</div>
</front>
</TEI>
<affiliations><list><country><li>Allemagne</li>
</country>
</list>
<tree><country name="Allemagne"><noRegion><name sortKey="Gerlach, M" sort="Gerlach, M" uniqKey="Gerlach M" first="M." last="Gerlach">M. Gerlach</name>
</noRegion>
<name sortKey="Gerlach, M" sort="Gerlach, M" uniqKey="Gerlach M" first="M." last="Gerlach">M. Gerlach</name>
<name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002209 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 002209 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonV1 |flux= Main |étape= Exploration |type= RBID |clé= ISTEX:64788B7E5263D0789468923A04FC1C66D18CF971 |texte= Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man }}
This area was generated with Dilib version V0.6.23. |