How to judge animal models of Parkinson's disease in terms of neuroprotection.
Identifieur interne : 000F03 ( PubMed/Corpus ); précédent : 000F02; suivant : 000F04How to judge animal models of Parkinson's disease in terms of neuroprotection.
Auteurs : E C HirschSource :
- Journal of neural transmission. Supplementum [ 0303-6995 ] ; 2006.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Neuroprotective Agents.
- chemical , toxicity : Neurotoxins.
- chemically induced : Parkinson Disease, Secondary.
- drug therapy : Parkinson Disease.
- genetics : Parkinson Disease.
- Animals, Disease Models, Animal, Humans.
Abstract
Ideally, animal models of Parkinson's should reproduce the clinical manifestation of the disease, a loss of some but not all dopaminergic neurons, a loss of some non dopaminergic neurons and alpha-synuclein positive inclusions resembling Lewy bodies. There are at least three ways to develop animal models of PD. The first two are based on the etiology of the disease and consist in 1) reproducing in animals the mutations seen in inherited forms of PD; 2) intoxicating animals with putative environmental toxins causing PD. The last method currently used, which is not exclusive of the first two, is to try to reproduce the molecular or biochemical changes seen post-mortem in the brain of patients with PD. In this review we discuss the advantages and the drawbacks in term of neuroprotection of the currently used models.
PubMed: 17017538
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pubmed:17017538Le document en format XML
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Supplementum</title><idno type="ISSN">0303-6995</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Neuroprotective Agents (therapeutic use)</term><term>Neurotoxins (toxicity)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease, Secondary (chemically induced)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Neurotoxins</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ideally, animal models of Parkinson's should reproduce the clinical manifestation of the disease, a loss of some but not all dopaminergic neurons, a loss of some non dopaminergic neurons and alpha-synuclein positive inclusions resembling Lewy bodies. There are at least three ways to develop animal models of PD. The first two are based on the etiology of the disease and consist in 1) reproducing in animals the mutations seen in inherited forms of PD; 2) intoxicating animals with putative environmental toxins causing PD. The last method currently used, which is not exclusive of the first two, is to try to reproduce the molecular or biochemical changes seen post-mortem in the brain of patients with PD. In this review we discuss the advantages and the drawbacks in term of neuroprotection of the currently used models.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17017538</PMID><DateCreated><Year>2006</Year><Month>10</Month><Day>04</Day></DateCreated><DateCompleted><Year>2006</Year><Month>10</Month><Day>24</Day></DateCompleted><DateRevised><Year>2006</Year><Month>10</Month><Day>04</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0303-6995</ISSN><JournalIssue CitedMedium="Print"><Issue>70</Issue><PubDate><Year>2006</Year></PubDate></JournalIssue><Title>Journal of neural transmission. Supplementum</Title><ISOAbbreviation>J. Neural Transm. 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In this review we discuss the advantages and the drawbacks in term of neuroprotection of the currently used models.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials><AffiliationInfo><Affiliation>INSERM U679, Hôpital de la Salpêtrière, Université Pierre et Marie Curie-Paris 6, Paris, France. hirsch@ccr.jussieu.fr</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Austria</Country><MedlineTA>J Neural Transm Suppl</MedlineTA><NlmUniqueID>0425126</NlmUniqueID><ISSNLinking>0303-6995</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009498">Neurotoxins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009498" MajorTopicYN="N">Neurotoxins</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>12</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>10</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>10</Month><Day>25</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>10</Month><Day>5</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17017538</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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