Animal models of Parkinson's disease: An updated overview.
Identifieur interne : 000413 ( PubMed/Checkpoint ); précédent : 000412; suivant : 000414Animal models of Parkinson's disease: An updated overview.
Auteurs : P. Gubellini [France] ; P. Kachidian [France]Source :
- Revue neurologique [ 0035-3787 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemically induced : Parkinson Disease, Secondary.
- genetics : Parkinson Disease.
- physiopathology : MPTP Poisoning, Parkinson Disease, Parkinson Disease, Secondary.
- Animals, Disease Models, Animal, Humans.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disorder whose etiology, besides a minority of genetic cases, is still largely unknown. Animal models have contributed to elucidate PD etiology and pathogenesis, as well as its cellular and molecular mechanisms, leading to the general hypothesis that this neurological disorder is due to complex interactions between environmental and genetic factors. However, the full understanding of PD is still very far from being achieved, and new potential treatments need to be tested to further improve patients' quality of life and, possibly, slow down the neurodegenerative process. In this context, animal models of PD are required to address all these issues. "Classic" models are based on neurotoxins that selectively target catecholaminergic neurons (such as 6-hydroxydopamine, 1-methyl-1,2,3,6-tetrahydropiridine, agricultural pesticides, etc.), while more recent models employ genetic manipulations that either introduce mutations similar to those find in familial cases of PD (α-synuclein, DJ-1, PINK1, Parkin, etc.) or selectively disrupt nigrostriatal neurons (MitoPark, Pitx3, Nurr1, etc.). Each one of these models has its own advantages and limitations, thus some are better suited for studying PD pathogenesis, while others are more pertinent to test therapeutic treatments. Here, we provide a critical and updated review of the most used PD models.
DOI: 10.1016/j.neurol.2015.07.011
PubMed: 26343921
Affiliations:
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Kachidian</name><affiliation wicri:level="4"><nlm:affiliation>Aix-Marseille Université, CNRS, Institut de Biologie du Développement de Marseille (IBDM) UMR7288, case 907, parc scientifique de Luminy, 163, avenue de Luminy, 13009 Marseille, France. 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Animal models have contributed to elucidate PD etiology and pathogenesis, as well as its cellular and molecular mechanisms, leading to the general hypothesis that this neurological disorder is due to complex interactions between environmental and genetic factors. However, the full understanding of PD is still very far from being achieved, and new potential treatments need to be tested to further improve patients' quality of life and, possibly, slow down the neurodegenerative process. In this context, animal models of PD are required to address all these issues. "Classic" models are based on neurotoxins that selectively target catecholaminergic neurons (such as 6-hydroxydopamine, 1-methyl-1,2,3,6-tetrahydropiridine, agricultural pesticides, etc.), while more recent models employ genetic manipulations that either introduce mutations similar to those find in familial cases of PD (α-synuclein, DJ-1, PINK1, Parkin, etc.) or selectively disrupt nigrostriatal neurons (MitoPark, Pitx3, Nurr1, etc.). Each one of these models has its own advantages and limitations, thus some are better suited for studying PD pathogenesis, while others are more pertinent to test therapeutic treatments. Here, we provide a critical and updated review of the most used PD models.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26343921</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>17</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>29</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0035-3787</ISSN><JournalIssue CitedMedium="Internet"><Volume>171</Volume><Issue>11</Issue><PubDate><Year>2015</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Revue neurologique</Title><ISOAbbreviation>Rev. Neurol. (Paris)</ISOAbbreviation></Journal><ArticleTitle>Animal models of Parkinson's disease: An updated overview.</ArticleTitle><Pagination><MedlinePgn>750-61</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neurol.2015.07.011</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0035-3787(15)00804-8</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a progressive neurodegenerative disorder whose etiology, besides a minority of genetic cases, is still largely unknown. Animal models have contributed to elucidate PD etiology and pathogenesis, as well as its cellular and molecular mechanisms, leading to the general hypothesis that this neurological disorder is due to complex interactions between environmental and genetic factors. However, the full understanding of PD is still very far from being achieved, and new potential treatments need to be tested to further improve patients' quality of life and, possibly, slow down the neurodegenerative process. In this context, animal models of PD are required to address all these issues. "Classic" models are based on neurotoxins that selectively target catecholaminergic neurons (such as 6-hydroxydopamine, 1-methyl-1,2,3,6-tetrahydropiridine, agricultural pesticides, etc.), while more recent models employ genetic manipulations that either introduce mutations similar to those find in familial cases of PD (α-synuclein, DJ-1, PINK1, Parkin, etc.) or selectively disrupt nigrostriatal neurons (MitoPark, Pitx3, Nurr1, etc.). Each one of these models has its own advantages and limitations, thus some are better suited for studying PD pathogenesis, while others are more pertinent to test therapeutic treatments. Here, we provide a critical and updated review of the most used PD models.</AbstractText><CopyrightInformation>Copyright © 2015 Elsevier Masson SAS. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gubellini</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Aix-Marseille Université, CNRS, Institut de Biologie du Développement de Marseille (IBDM) UMR7288, case 907, parc scientifique de Luminy, 163, avenue de Luminy, 13009 Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kachidian</LastName><ForeName>P</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Aix-Marseille Université, CNRS, Institut de Biologie du Développement de Marseille (IBDM) UMR7288, case 907, parc scientifique de Luminy, 163, avenue de Luminy, 13009 Marseille, France. Electronic address: philippe.kachidian@univ-amu.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>09</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Rev Neurol (Paris)</MedlineTA><NlmUniqueID>2984779R</NlmUniqueID><ISSNLinking>0035-3787</ISSNLinking></MedlineJournalInfo><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="D020267" MajorTopicYN="N">MPTP Poisoning</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Corps de Lewy</Keyword><Keyword MajorTopicYN="N">Dopamine</Keyword><Keyword MajorTopicYN="N">Lewy bodies</Keyword><Keyword MajorTopicYN="N">Neurodegeneration</Keyword><Keyword MajorTopicYN="N">Neurodégénérescence</Keyword><Keyword MajorTopicYN="N">Nigrostriatal</Keyword><Keyword MajorTopicYN="N">Pathologie progressive</Keyword><Keyword MajorTopicYN="N">Progressive disease</Keyword><Keyword MajorTopicYN="N">Voie nigrostriée</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>05</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>07</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>07</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>9</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>9</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>8</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26343921</ArticleId><ArticleId IdType="pii">S0035-3787(15)00804-8</ArticleId><ArticleId IdType="doi">10.1016/j.neurol.2015.07.011</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Provence-Alpes-Côte d'Azur</li></region><settlement><li>Marseille</li></settlement><orgName><li>Université d'Aix-Marseille</li></orgName></list><tree><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Gubellini, P" sort="Gubellini, P" uniqKey="Gubellini P" first="P" last="Gubellini">P. Gubellini</name></region><name sortKey="Kachidian, P" sort="Kachidian, P" uniqKey="Kachidian P" first="P" last="Kachidian">P. Kachidian</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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