Animal models of Parkinson's disease: a gateway to therapeutics?
Identifieur interne : 000037 ( PubMed/Curation ); précédent : 000036; suivant : 000038Animal models of Parkinson's disease: a gateway to therapeutics?
Auteurs : Weidong Le [République populaire de Chine] ; Pavani Sayana ; Joseph JankovicSource :
- Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics ; 2014.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Antiparkinson Agents.
- etiology : Parkinson Disease.
- therapy : Parkinson Disease.
- Animals, Disease Models, Animal, Drug Evaluation, Preclinical, Humans.
Abstract
Parkinson's disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various in vivo models of PD used to test novel therapeutic strategies.
DOI: 10.1007/s13311-013-0234-1
PubMed: 24158912
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Animal models of Parkinson's disease: a gateway to therapeutics?</title><author><name sortKey="Le, Weidong" sort="Le, Weidong" uniqKey="Le W" first="Weidong" last="Le">Weidong Le</name><affiliation wicri:level="1"><nlm:affiliation>1st Affiliated Hospital, Dalian Medical University, Dalian, 116011, China, wdle@sibs.ac.cn.</nlm:affiliation><country wicri:rule="url">République populaire de Chine</country><wicri:regionArea>1st Affiliated Hospital, Dalian Medical University, Dalian, 116011, China</wicri:regionArea></affiliation></author><author><name sortKey="Sayana, Pavani" sort="Sayana, Pavani" uniqKey="Sayana P" first="Pavani" last="Sayana">Pavani Sayana</name></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="doi">10.1007/s13311-013-0234-1</idno><idno type="RBID">pubmed:24158912</idno><idno type="pmid">24158912</idno><idno type="wicri:Area/PubMed/Corpus">000037</idno><idno type="wicri:Area/PubMed/Curation">000037</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Animal models of Parkinson's disease: a gateway to therapeutics?</title><author><name sortKey="Le, Weidong" sort="Le, Weidong" uniqKey="Le W" first="Weidong" last="Le">Weidong Le</name><affiliation wicri:level="1"><nlm:affiliation>1st Affiliated Hospital, Dalian Medical University, Dalian, 116011, China, wdle@sibs.ac.cn.</nlm:affiliation><country wicri:rule="url">République populaire de Chine</country><wicri:regionArea>1st Affiliated Hospital, Dalian Medical University, Dalian, 116011, China</wicri:regionArea></affiliation></author><author><name sortKey="Sayana, Pavani" sort="Sayana, Pavani" uniqKey="Sayana P" first="Pavani" last="Sayana">Pavani Sayana</name></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name></author></analytic><series><title level="j">Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics</title><idno type="e-ISSN">1878-7479</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (therapeutic use)</term><term>Disease Models, Animal</term><term>Drug Evaluation, Preclinical</term><term>Humans</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (therapy)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Drug Evaluation, Preclinical</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various in vivo models of PD used to test novel therapeutic strategies.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">24158912</PMID><DateCreated><Year>2014</Year><Month>01</Month><Day>23</Day></DateCreated><DateCompleted><Year>2014</Year><Month>09</Month><Day>19</Day></DateCompleted><DateRevised><Year>2015</Year><Month>04</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1878-7479</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>1</Issue><PubDate><Year>2014</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics</Title><ISOAbbreviation>Neurotherapeutics</ISOAbbreviation></Journal><ArticleTitle>Animal models of Parkinson's disease: a gateway to therapeutics?</ArticleTitle><Pagination><MedlinePgn>92-110</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s13311-013-0234-1</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various in vivo models of PD used to test novel therapeutic strategies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Le</LastName><ForeName>Weidong</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>1st Affiliated Hospital, Dalian Medical University, Dalian, 116011, China, wdle@sibs.ac.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sayana</LastName><ForeName>Pavani</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Jankovic</LastName><ForeName>Joseph</ForeName><Initials>J</Initials></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></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurotherapeutics</MedlineTA><NlmUniqueID>101290381</NlmUniqueID><ISSNLinking>1878-7479</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Neurosci Lett. 2012 Jul 11;521(1):15-9</RefSource><PMID Version="1">22617635</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2012 Jul;135(Pt 7):2058-73</RefSource><PMID Version="1">22719003</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Opin Neurol. 2012 Aug;25(4):433-47</RefSource><PMID Version="1">22691758</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Curr Opin Neurol. 2012 Aug;25(4):448-59</RefSource><PMID Version="1">22772874</PMID></CommentsCorrections><CommentsCorrections 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Evaluation, Preclinical</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000628">therapy</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3899493</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>10</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>10</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>9</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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