Engineering animal models of dystonia.
Identifieur interne : 000A09 ( PubMed/Checkpoint ); précédent : 000A08; suivant : 000A10Engineering animal models of dystonia.
Auteurs : Janneth Oleas [États-Unis] ; Fumiaki Yokoi ; Mark P. Deandrade ; Antonio Pisani ; Yuqing LiSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Molecular Chaperones.
- genetics : Dystonia.
- metabolism : Brain.
- pathology : Brain, Dystonia.
- Animals, Animals, Genetically Modified, Bioengineering, Disease Models, Animal, Drug Evaluation, Preclinical, Humans.
Abstract
Dystonia is a neurological disorder characterized by abnormal involuntary movements that are prolonged and often cause twisting and turning. Several genetically modified worms, fruit flies, and rodents have been generated as models of genetic dystonias, in particular DYT1, DYT11, and DYT12 dystonias. Although these models do not show overt dystonic symptoms, the rodent models exhibit motor deficits in specialized behavioral tasks, such as the rotarod and beam-walking tests. For example, in a rodent model of DYT12 dystonia, which is generally stress triggered, motor deficits are observed only after the animal is stressed. Moreover, in a rodent model of DYT1 dystonia, the motor and electrophysiological deficits can be rescued by trihexyphenidyl, a common anticholinergic medication used to treat dystonic symptoms in human patients. Biochemically, the DYT1 and DYT11 animal models also share some similarities to patients, such as a reduction in striatal D2 dopamine receptor and binding activities. In addition, conditional knockout mouse models for DYT1 and DYT11 dystonia demonstrate that loss of the causal dystonia-related proteins in the striatum leads to motor deficits. Interestingly, loss of the DYT1 dystonia causal protein in Purkinje cells shows an improvement in motor performance, suggesting that gene therapy targeting of the cerebellum or intervention in its downstream pathways may be useful. Finally, recent studies using DYT1 dystonia worm and mouse models led to a potential novel therapeutic agent, which is currently undergoing clinical trials. These results indicate that genetic animal models are powerful tools to elucidate the pathophysiology and to further develop new therapeutics for dystonia.
DOI: 10.1002/mds.25583
PubMed: 23893455
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Engineering animal models of dystonia.</title><author><name sortKey="Oleas, Janneth" sort="Oleas, Janneth" uniqKey="Oleas J" first="Janneth" last="Oleas">Janneth Oleas</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, College of Medicine, University of Florida, Gainesville, Florida 32610, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, College of Medicine, University of Florida, Gainesville, Florida 32610</wicri:regionArea><wicri:noRegion>Florida 32610</wicri:noRegion></affiliation></author><author><name sortKey="Yokoi, Fumiaki" sort="Yokoi, Fumiaki" uniqKey="Yokoi F" first="Fumiaki" last="Yokoi">Fumiaki Yokoi</name></author><author><name sortKey="Deandrade, Mark P" sort="Deandrade, Mark P" uniqKey="Deandrade M" first="Mark P" last="Deandrade">Mark P. Deandrade</name></author><author><name sortKey="Pisani, Antonio" sort="Pisani, Antonio" uniqKey="Pisani A" first="Antonio" last="Pisani">Antonio Pisani</name></author><author><name sortKey="Li, Yuqing" sort="Li, Yuqing" uniqKey="Li Y" first="Yuqing" last="Li">Yuqing Li</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="doi">10.1002/mds.25583</idno><idno type="RBID">pubmed:23893455</idno><idno type="pmid">23893455</idno><idno type="wicri:Area/PubMed/Corpus">000802</idno><idno type="wicri:Area/PubMed/Curation">000802</idno><idno type="wicri:Area/PubMed/Checkpoint">000A09</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Engineering animal models of dystonia.</title><author><name sortKey="Oleas, Janneth" sort="Oleas, Janneth" uniqKey="Oleas J" first="Janneth" last="Oleas">Janneth Oleas</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, College of Medicine, University of Florida, Gainesville, Florida 32610, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, College of Medicine, University of Florida, Gainesville, Florida 32610</wicri:regionArea><wicri:noRegion>Florida 32610</wicri:noRegion></affiliation></author><author><name sortKey="Yokoi, Fumiaki" sort="Yokoi, Fumiaki" uniqKey="Yokoi F" first="Fumiaki" last="Yokoi">Fumiaki Yokoi</name></author><author><name sortKey="Deandrade, Mark P" sort="Deandrade, Mark P" uniqKey="Deandrade M" first="Mark P" last="Deandrade">Mark P. Deandrade</name></author><author><name sortKey="Pisani, Antonio" sort="Pisani, Antonio" uniqKey="Pisani A" first="Antonio" last="Pisani">Antonio Pisani</name></author><author><name sortKey="Li, Yuqing" sort="Li, Yuqing" uniqKey="Li Y" first="Yuqing" last="Li">Yuqing Li</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>Animals, Genetically Modified</term><term>Bioengineering</term><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Disease Models, Animal</term><term>Drug Evaluation, Preclinical</term><term>Dystonia (genetics)</term><term>Dystonia (pathology)</term><term>Humans</term><term>Molecular Chaperones (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Molecular Chaperones</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dystonia</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Dystonia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Genetically Modified</term><term>Bioengineering</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">Dystonia is a neurological disorder characterized by abnormal involuntary movements that are prolonged and often cause twisting and turning. Several genetically modified worms, fruit flies, and rodents have been generated as models of genetic dystonias, in particular DYT1, DYT11, and DYT12 dystonias. Although these models do not show overt dystonic symptoms, the rodent models exhibit motor deficits in specialized behavioral tasks, such as the rotarod and beam-walking tests. For example, in a rodent model of DYT12 dystonia, which is generally stress triggered, motor deficits are observed only after the animal is stressed. Moreover, in a rodent model of DYT1 dystonia, the motor and electrophysiological deficits can be rescued by trihexyphenidyl, a common anticholinergic medication used to treat dystonic symptoms in human patients. Biochemically, the DYT1 and DYT11 animal models also share some similarities to patients, such as a reduction in striatal D2 dopamine receptor and binding activities. In addition, conditional knockout mouse models for DYT1 and DYT11 dystonia demonstrate that loss of the causal dystonia-related proteins in the striatum leads to motor deficits. Interestingly, loss of the DYT1 dystonia causal protein in Purkinje cells shows an improvement in motor performance, suggesting that gene therapy targeting of the cerebellum or intervention in its downstream pathways may be useful. Finally, recent studies using DYT1 dystonia worm and mouse models led to a potential novel therapeutic agent, which is currently undergoing clinical trials. These results indicate that genetic animal models are powerful tools to elucidate the pathophysiology and to further develop new therapeutics for dystonia.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23893455</PMID><DateCreated><Year>2013</Year><Month>07</Month><Day>29</Day></DateCreated><DateCompleted><Year>2014</Year><Month>02</Month><Day>26</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>7</Issue><PubDate><Year>2013</Year><Month>Jun</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Engineering animal models of dystonia.</ArticleTitle><Pagination><MedlinePgn>990-1000</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25583</ELocationID><Abstract><AbstractText>Dystonia is a neurological disorder characterized by abnormal involuntary movements that are prolonged and often cause twisting and turning. Several genetically modified worms, fruit flies, and rodents have been generated as models of genetic dystonias, in particular DYT1, DYT11, and DYT12 dystonias. Although these models do not show overt dystonic symptoms, the rodent models exhibit motor deficits in specialized behavioral tasks, such as the rotarod and beam-walking tests. For example, in a rodent model of DYT12 dystonia, which is generally stress triggered, motor deficits are observed only after the animal is stressed. Moreover, in a rodent model of DYT1 dystonia, the motor and electrophysiological deficits can be rescued by trihexyphenidyl, a common anticholinergic medication used to treat dystonic symptoms in human patients. Biochemically, the DYT1 and DYT11 animal models also share some similarities to patients, such as a reduction in striatal D2 dopamine receptor and binding activities. In addition, conditional knockout mouse models for DYT1 and DYT11 dystonia demonstrate that loss of the causal dystonia-related proteins in the striatum leads to motor deficits. Interestingly, loss of the DYT1 dystonia causal protein in Purkinje cells shows an improvement in motor performance, suggesting that gene therapy targeting of the cerebellum or intervention in its downstream pathways may be useful. Finally, recent studies using DYT1 dystonia worm and mouse models led to a potential novel therapeutic agent, which is currently undergoing clinical trials. These results indicate that genetic animal models are powerful tools to elucidate the pathophysiology and to further develop new therapeutics for dystonia.</AbstractText><CopyrightInformation>© 2013 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Oleas</LastName><ForeName>Janneth</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Neurology, College of Medicine, University of Florida, Gainesville, Florida 32610, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yokoi</LastName><ForeName>Fumiaki</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>DeAndrade</LastName><ForeName>Mark P</ForeName><Initials>MP</Initials></Author><Author ValidYN="Y"><LastName>Pisani</LastName><ForeName>Antonio</ForeName><Initials>A</Initials></Author><Author 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States</Country></Grant><Grant><GrantID>NS74423</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 NS057098</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS037409</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS054246</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R03 NS074423</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS042356</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS047692</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS065273</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 NS072872</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., Extramural</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>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018832">Molecular Chaperones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C108175">TOR1A protein, 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MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004195">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004353">Drug Evaluation, Preclinical</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004421">Dystonia</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018832">Molecular Chaperones</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS513931</OtherID><OtherID Source="NLM">PMC3800691</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">DYT1</Keyword><Keyword MajorTopicYN="N">DYT11</Keyword><Keyword MajorTopicYN="N">DYT12</Keyword><Keyword MajorTopicYN="N">animal model</Keyword><Keyword MajorTopicYN="N">dystonia</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year><Month>12</Month><Day>7</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2013</Year><Month>5</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2013</Year><Month>5</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>7</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>7</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>2</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.25583</ArticleId><ArticleId IdType="pubmed">23893455</ArticleId><ArticleId IdType="pmc">PMC3800691</ArticleId><ArticleId IdType="mid">NIHMS513931</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Deandrade, Mark P" sort="Deandrade, Mark P" uniqKey="Deandrade M" first="Mark P" last="Deandrade">Mark P. Deandrade</name><name sortKey="Li, Yuqing" sort="Li, Yuqing" uniqKey="Li Y" first="Yuqing" last="Li">Yuqing Li</name><name sortKey="Pisani, Antonio" sort="Pisani, Antonio" uniqKey="Pisani A" first="Antonio" last="Pisani">Antonio Pisani</name><name sortKey="Yokoi, Fumiaki" sort="Yokoi, Fumiaki" uniqKey="Yokoi F" first="Fumiaki" last="Yokoi">Fumiaki Yokoi</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Oleas, Janneth" sort="Oleas, Janneth" uniqKey="Oleas J" first="Janneth" last="Oleas">Janneth Oleas</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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