MovDisordV3, PubMed, Checkpoint, bibRecord, 000B14

Animal models for dystonia.

Identifieur interne : 000B14 ( PubMed/Checkpoint ); précédent : 000B13; suivant : 000B15

Animal models for dystonia.

Auteurs : Bethany K. Wilson [États-Unis] ; Ellen J. Hess

Source :

Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.

RBID : pubmed:23893454

English descriptors

KwdEn :
- Animals, Animals, Genetically Modified, Basal Ganglia (pathology), Disease Models, Animal, Dystonia (complications), Dystonia (genetics), Dystonia (pathology), Humans, Neurotransmitter Agents (genetics), Neurotransmitter Agents (metabolism).
MESH :
- chemical , genetics : Neurotransmitter Agents.
- complications : Dystonia.
- genetics : Dystonia.
- chemical , metabolism : Neurotransmitter Agents.
- pathology : Basal Ganglia, Dystonia.
- Animals, Animals, Genetically Modified, Disease Models, Animal, Humans.

Abstract

Symptomatic animal models have clinical features consistent with human disorders and are often used to identify the anatomical and physiological processes involved in the expression of symptoms and to experimentally demonstrate causality where it would be infeasible in the patient population. Rodent and primate models of dystonia have identified basal ganglia abnormalities, including alterations in striatal GABAergic (ie, transmitting or secreting γ-aminobutyric acid) and dopaminergic transmission. Symptomatic animal models have also established the critical role of the cerebellum in dystonia, particularly abnormal glutamate signaling and aberrant Purkinje cell activity. Further, experiments suggest that the basal ganglia and cerebellum are nodes in an integrated network that is dysfunctional in dystonia. The knowledge gained from experiments in symptomatic animal models may serve as the foundation for the development of novel therapeutic interventions to treat dystonia. © 2013 Movement Disorder Society.

DOI: 10.1002/mds.25526
PubMed: 23893454

Affiliations:

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 000803
to stream PubMed, to step Curation: 000803

Links to Exploration step

pubmed:23893454

Le document en format XML

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<author><name sortKey="Wilson, Bethany K" sort="Wilson, Bethany K" uniqKey="Wilson B" first="Bethany K" last="Wilson">Bethany K. Wilson</name>
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<author><name sortKey="Hess, Ellen J" sort="Hess, Ellen J" uniqKey="Hess E" first="Ellen J" last="Hess">Ellen J. Hess</name>
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<term>Dystonia (complications)</term>
<term>Dystonia (genetics)</term>
<term>Dystonia (pathology)</term>
<term>Humans</term>
<term>Neurotransmitter Agents (genetics)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Neurotransmitter Agents</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dystonia</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Neurotransmitter Agents</term>
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<term>Dystonia</term>
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<front><div type="abstract" xml:lang="en">Symptomatic animal models have clinical features consistent with human disorders and are often used to identify the anatomical and physiological processes involved in the expression of symptoms and to experimentally demonstrate causality where it would be infeasible in the patient population. Rodent and primate models of dystonia have identified basal ganglia abnormalities, including alterations in striatal GABAergic (ie, transmitting or secreting γ-aminobutyric acid) and dopaminergic transmission. Symptomatic animal models have also established the critical role of the cerebellum in dystonia, particularly abnormal glutamate signaling and aberrant Purkinje cell activity. Further, experiments suggest that the basal ganglia and cerebellum are nodes in an integrated network that is dysfunctional in dystonia. The knowledge gained from experiments in symptomatic animal models may serve as the foundation for the development of novel therapeutic interventions to treat dystonia. © 2013 Movement Disorder Society.</div>
</front>
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<Abstract><AbstractText>Symptomatic animal models have clinical features consistent with human disorders and are often used to identify the anatomical and physiological processes involved in the expression of symptoms and to experimentally demonstrate causality where it would be infeasible in the patient population. Rodent and primate models of dystonia have identified basal ganglia abnormalities, including alterations in striatal GABAergic (ie, transmitting or secreting γ-aminobutyric acid) and dopaminergic transmission. Symptomatic animal models have also established the critical role of the cerebellum in dystonia, particularly abnormal glutamate signaling and aberrant Purkinje cell activity. Further, experiments suggest that the basal ganglia and cerebellum are nodes in an integrated network that is dysfunctional in dystonia. The knowledge gained from experiments in symptomatic animal models may serve as the foundation for the development of novel therapeutic interventions to treat dystonia. © 2013 Movement Disorder Society.</AbstractText>
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<MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D030801">Animals, Genetically Modified</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D001479">Basal Ganglia</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004195">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004421">Dystonia</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName>
<QualifierName MajorTopicYN="N" 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="D018377">Neurotransmitter Agents</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<OtherID Source="NLM">NIHMS476580</OtherID>
<OtherID Source="NLM">PMC3728703</OtherID>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">basal ganglia</Keyword>
<Keyword MajorTopicYN="N">cerebellum</Keyword>
<Keyword MajorTopicYN="N">mouse model</Keyword>
<Keyword MajorTopicYN="N">primate model</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year>
<Month>1</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2013</Year>
<Month>3</Month>
<Day>19</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2013</Year>
<Month>4</Month>
<Day>29</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2013</Year>
<Month>7</Month>
<Day>30</Day>
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<PubMedPubDate PubStatus="pubmed"><Year>2013</Year>
<Month>7</Month>
<Day>31</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="medline"><Year>2014</Year>
<Month>2</Month>
<Day>27</Day>
<Hour>6</Hour>
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</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="doi">10.1002/mds.25526</ArticleId>
<ArticleId IdType="pubmed">23893454</ArticleId>
<ArticleId IdType="pmc">PMC3728703</ArticleId>
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<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Géorgie (États-Unis)</li>
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<tree><noCountry><name sortKey="Hess, Ellen J" sort="Hess, Ellen J" uniqKey="Hess E" first="Ellen J" last="Hess">Ellen J. Hess</name>
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<country name="États-Unis"><region name="Géorgie (États-Unis)"><name sortKey="Wilson, Bethany K" sort="Wilson, Bethany K" uniqKey="Wilson B" first="Bethany K" last="Wilson">Bethany K. Wilson</name>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Animal models for dystonia.

Animal models for dystonia.

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