New animal models of Parkinson's disease.
Identifieur interne : 000F71 ( PubMed/Corpus ); précédent : 000F70; suivant : 000F72New animal models of Parkinson's disease.
Auteurs : Benjamin Dehay ; Erwan BezardSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- MESH :
Abstract
Parkinson's disease is a progressive neurodegenerative disorder mainly characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in the affected brain regions, of protein inclusions named Lewy Bodies. Despite the fact that numerous mutations causing hereditary forms of Parkinson's disease have been identified in the last decade, current transgenic animal models do not adequately reproduce cardinal features of the human disease. Altogether, the animal models derived of human mutations indicate that the nigrostriatal degenerative process results from the combination of several mechanisms that implicate mitochondrial dysfunction, oxidative damage, and protein degradation impairment.
PubMed: 22046592
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pubmed:22046592Le document en format XML
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<author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name>
<affiliation><nlm:affiliation>Université Victor Ségalen-Bordeaux II, Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Bordeaux, France. benjamin.dehay@u-bordeaux2.fr</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name>
</author>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">New animal models of Parkinson's disease.</title>
<author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name>
<affiliation><nlm:affiliation>Université Victor Ségalen-Bordeaux II, Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Bordeaux, France. benjamin.dehay@u-bordeaux2.fr</nlm:affiliation>
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</author>
<author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="eISSN">1531-8257</idno>
<imprint><date when="2011" type="published">2011</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Caenorhabditis elegans</term>
<term>Disease Models, Animal</term>
<term>Drosophila melanogaster</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
<term>Parkinson Disease (genetics)</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>Caenorhabditis elegans</term>
<term>Disease Models, Animal</term>
<term>Drosophila melanogaster</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease is a progressive neurodegenerative disorder mainly characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in the affected brain regions, of protein inclusions named Lewy Bodies. Despite the fact that numerous mutations causing hereditary forms of Parkinson's disease have been identified in the last decade, current transgenic animal models do not adequately reproduce cardinal features of the human disease. Altogether, the animal models derived of human mutations indicate that the nigrostriatal degenerative process results from the combination of several mechanisms that implicate mitochondrial dysfunction, oxidative damage, and protein degradation impairment.</div>
</front>
</TEI>
<pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">22046592</PMID>
<DateCreated><Year>2011</Year>
<Month>10</Month>
<Day>31</Day>
</DateCreated>
<DateCompleted><Year>2011</Year>
<Month>11</Month>
<Day>02</Day>
</DateCompleted>
<DateRevised><Year>2014</Year>
<Month>07</Month>
<Day>30</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>26</Volume>
<Issue>7</Issue>
<PubDate><Year>2011</Year>
<Month>Jun</Month>
</PubDate>
</JournalIssue>
<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
<ISOAbbreviation>Mov. Disord.</ISOAbbreviation>
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<ArticleTitle>New animal models of Parkinson's disease.</ArticleTitle>
<Pagination><MedlinePgn>1198-1205</MedlinePgn>
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<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Parkinson's disease is a progressive neurodegenerative disorder mainly characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in the affected brain regions, of protein inclusions named Lewy Bodies. Despite the fact that numerous mutations causing hereditary forms of Parkinson's disease have been identified in the last decade, current transgenic animal models do not adequately reproduce cardinal features of the human disease. Altogether, the animal models derived of human mutations indicate that the nigrostriatal degenerative process results from the combination of several mechanisms that implicate mitochondrial dysfunction, oxidative damage, and protein degradation impairment.</AbstractText>
<AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">We performed a literature search between 2008 and 2010.</AbstractText>
<AbstractText Label="DISCUSSION" NlmCategory="CONCLUSIONS">The absence of adequate in vivo experimental models of Parkinson's disease has severe repercussions for therapeutic intervention success for this incurable neurodegenerative disorder. The present nonexhaustive review looks at invertebrate and mammalian models of Parkinson's disease generated in the last three years.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dehay</LastName>
<ForeName>Benjamin</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Université Victor Ségalen-Bordeaux II, Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Bordeaux, France. benjamin.dehay@u-bordeaux2.fr</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bezard</LastName>
<ForeName>Erwan</ForeName>
<Initials>E</Initials>
</Author>
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<Language>eng</Language>
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<MedlineJournalInfo><Country>United States</Country>
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<MeshHeading><DescriptorName MajorTopicYN="N" UI="D051379">Mice</DescriptorName>
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<MeshHeading><DescriptorName MajorTopicYN="N" UI="D008822">Mice, Transgenic</DescriptorName>
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</MeshHeading>
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