Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.
Identifieur interne : 000735 ( PubMed/Checkpoint ); précédent : 000734; suivant : 000736Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.
Auteurs : Erwan Bezard [France] ; Zhenyu Yue ; Deniz Kirik ; Maria Grazia SpillantiniSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Genetic Vectors (adverse effects), Humans, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Mice, Mice, Transgenic, Mutation (genetics), Neuroprotective Agents (therapeutic use), Neurotoxins (toxicity), Parkinson Disease (drug therapy), Parkinson Disease (etiology), Protein-Serine-Threonine Kinases (genetics), alpha-Synuclein (genetics).
- MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases, alpha-Synuclein.
- chemical , therapeutic use : Neuroprotective Agents.
- chemical , toxicity : Neurotoxins.
- chemical : Leucine-Rich Repeat Serine-Threonine Protein Kinase-2.
- adverse effects : Genetic Vectors.
- drug therapy : Parkinson Disease.
- etiology : Parkinson Disease.
- genetics : Mutation.
- Animals, Disease Models, Animal, Humans, Mice, Mice, Transgenic.
Abstract
Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology and pathogenesis of Parkinson's disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modeling PD revolves around what can be called the disease gene-based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine-producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease-related genes. In this position article, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that, we argue, should be utilized in the preclinical development phase of new neuroprotective therapies before embarking into clinical trials.
DOI: 10.1002/mds.25108
PubMed: 22753348
Affiliations:
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pubmed:22753348Le document en format XML
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uniqKey="Kirik D" first="Deniz" last="Kirik">Deniz Kirik</name></author><author><name sortKey="Spillantini, Maria Grazia" sort="Spillantini, Maria Grazia" uniqKey="Spillantini M" first="Maria Grazia" last="Spillantini">Maria Grazia Spillantini</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:22753348</idno><idno type="pmid">22753348</idno><idno type="doi">10.1002/mds.25108</idno><idno type="wicri:Area/PubMed/Corpus">000798</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000798</idno><idno type="wicri:Area/PubMed/Curation">000762</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000762</idno><idno type="wicri:Area/PubMed/Checkpoint">000762</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000762</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.</title><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation wicri:level="3"><nlm:affiliation>University de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux, France. erwan.bezard@u-bordeaux2.fr</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>University de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux</wicri:regionArea><placeName><region type="region">Nouvelle-Aquitaine</region><region type="old region">Aquitaine</region><settlement type="city">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name></author><author><name sortKey="Kirik, Deniz" sort="Kirik, Deniz" uniqKey="Kirik D" first="Deniz" last="Kirik">Deniz Kirik</name></author><author><name sortKey="Spillantini, Maria Grazia" sort="Spillantini, Maria Grazia" uniqKey="Spillantini M" first="Maria Grazia" last="Spillantini">Maria Grazia Spillantini</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Genetic Vectors (adverse effects)</term><term>Humans</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term><term>Mice</term><term>Mice, Transgenic</term><term>Mutation (genetics)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Neurotoxins (toxicity)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (etiology)</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>alpha-Synuclein (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term><term>alpha-Synuclein</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" type="chemical" xml:lang="en"><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Genetic Vectors</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Mice</term><term>Mice, Transgenic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology and pathogenesis of Parkinson's disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modeling PD revolves around what can be called the disease gene-based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine-producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease-related genes. In this position article, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that, we argue, should be utilized in the preclinical development phase of new neuroprotective therapies before embarking into clinical trials.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22753348</PMID><DateCreated><Year>2013</Year><Month>02</Month><Day>07</Day></DateCreated><DateCompleted><Year>2013</Year><Month>08</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>1</Issue><PubDate><Year>2013</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Animal models of Parkinson's disease: limits and relevance to neuroprotection studies.</ArticleTitle><Pagination><MedlinePgn>61-70</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25108</ELocationID><Abstract><AbstractText>Over the last two decades, significant strides has been made toward acquiring a better knowledge of both the etiology and pathogenesis of Parkinson's disease (PD). Experimental models are of paramount importance to obtain greater insights into the pathogenesis of the disease. Thus far, neurotoxin-based animal models have been the most popular tools employed to produce selective neuronal death in both in vitro and in vivo systems. These models have been commonly referred to as the pathogenic models. The current trend in modeling PD revolves around what can be called the disease gene-based models or etiologic models. The value of utilizing multiple models with a different mechanism of insult rests on the premise that dopamine-producing neurons die by stereotyped cascades that can be activated by a range of insults, from neurotoxins to downregulation and overexpression of disease-related genes. In this position article, we present the relevance of both pathogenic and etiologic models as well as the concept of clinically relevant designs that, we argue, should be utilized in the preclinical development phase of new neuroprotective therapies before embarking into clinical trials.</AbstractText><CopyrightInformation>Copyright © 2013 Movement Disorders Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>Erwan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>University de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, Bordeaux, France. erwan.bezard@u-bordeaux2.fr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yue</LastName><ForeName>Zhenyu</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Kirik</LastName><ForeName>Deniz</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Spillantini</LastName><ForeName>Maria Grazia</ForeName><Initials>MG</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G-1102</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>242932</GrantID><Agency>European Research Council</Agency><Country>International</Country></Grant><Grant><GrantID>R01 NS072359</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS060809</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS072359-01</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS060809-01</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., 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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="Q000209" MajorTopicYN="Y">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS386110</OtherID><OtherID Source="NLM">PMC3517687</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>04</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2012</Year><Month>05</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2012</Year><Month>06</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2012</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>8</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22753348</ArticleId><ArticleId IdType="doi">10.1002/mds.25108</ArticleId><ArticleId IdType="pmc">PMC3517687</ArticleId><ArticleId IdType="mid">NIHMS386110</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li></country><region><li>Aquitaine</li><li>Nouvelle-Aquitaine</li></region><settlement><li>Bordeaux</li></settlement></list><tree><noCountry><name sortKey="Kirik, Deniz" sort="Kirik, Deniz" uniqKey="Kirik D" first="Deniz" last="Kirik">Deniz Kirik</name><name sortKey="Spillantini, Maria Grazia" sort="Spillantini, Maria Grazia" uniqKey="Spillantini M" first="Maria Grazia" last="Spillantini">Maria Grazia Spillantini</name><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name></noCountry><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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