Alpha-synuclein-based models of Parkinson's disease.
Identifieur interne : 000138 ( PubMed/Corpus ); précédent : 000137; suivant : 000139Alpha-synuclein-based models of Parkinson's disease.
Auteurs : B. Dehay ; P-O FernagutSource :
- Revue neurologique [ 0035-3787 ]
Abstract
Parkinson's disease is a progressive neurodegenerative disorder mainly characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in the affected brain regions, of protein inclusions called 'Lewy bodies'. Most cases are sporadic, but mutations in several genes, including SNCA, which encodes α-synuclein, are associated with disease development. A myriad of α-synuclein-based models for studying Parkinson's disease have been generated over the last two decades through different methodologies. Collectively, these models offer new opportunities to elucidate the mechanisms underlying the relentless progression of protein aggregation and neurodegeneration in Parkinson's. The present, non-exhaustive review focuses on mammalian models and the main strategies that are currently available, including transgenesis, viral vector gene delivery and the recently developed 'prion-like' models.
DOI: 10.1016/j.neurol.2016.04.003
PubMed: 27158042
Links to Exploration step
pubmed:27158042Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Alpha-synuclein-based models of Parkinson's disease.</title>
<author><name sortKey="Dehay, B" sort="Dehay, B" uniqKey="Dehay B" first="B" last="Dehay">B. Dehay</name>
<affiliation><nlm:affiliation>Institut des maladies neurodégénératives, université de Bordeaux, UMR 5293, 33000 Bordeaux, France; CNRS, institut des maladies neurodégénératives, UMR 5293, 33000 Bordeaux, France. Electronic address: benjamin.dehay@u-bordeaux.fr.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Fernagut, P O" sort="Fernagut, P O" uniqKey="Fernagut P" first="P-O" last="Fernagut">P-O Fernagut</name>
<affiliation><nlm:affiliation>Institut des maladies neurodégénératives, université de Bordeaux, UMR 5293, 33000 Bordeaux, France; CNRS, institut des maladies neurodégénératives, UMR 5293, 33000 Bordeaux, France.</nlm:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="????"><PubDate><MedlineDate>2016 Jun-Jul</MedlineDate>
</PubDate>
</date>
<idno type="RBID">pubmed:27158042</idno>
<idno type="pmid">27158042</idno>
<idno type="doi">10.1016/j.neurol.2016.04.003</idno>
<idno type="wicri:Area/PubMed/Corpus">000138</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000138</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Alpha-synuclein-based models of Parkinson's disease.</title>
<author><name sortKey="Dehay, B" sort="Dehay, B" uniqKey="Dehay B" first="B" last="Dehay">B. Dehay</name>
<affiliation><nlm:affiliation>Institut des maladies neurodégénératives, université de Bordeaux, UMR 5293, 33000 Bordeaux, France; CNRS, institut des maladies neurodégénératives, UMR 5293, 33000 Bordeaux, France. Electronic address: benjamin.dehay@u-bordeaux.fr.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Fernagut, P O" sort="Fernagut, P O" uniqKey="Fernagut P" first="P-O" last="Fernagut">P-O Fernagut</name>
<affiliation><nlm:affiliation>Institut des maladies neurodégénératives, université de Bordeaux, UMR 5293, 33000 Bordeaux, France; CNRS, institut des maladies neurodégénératives, UMR 5293, 33000 Bordeaux, France.</nlm:affiliation>
</affiliation>
</author>
</analytic>
<series><title level="j">Revue neurologique</title>
<idno type="ISSN">0035-3787</idno>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Parkinson's disease is a progressive neurodegenerative disorder mainly characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in the affected brain regions, of protein inclusions called 'Lewy bodies'. Most cases are sporadic, but mutations in several genes, including SNCA, which encodes α-synuclein, are associated with disease development. A myriad of α-synuclein-based models for studying Parkinson's disease have been generated over the last two decades through different methodologies. Collectively, these models offer new opportunities to elucidate the mechanisms underlying the relentless progression of protein aggregation and neurodegeneration in Parkinson's. The present, non-exhaustive review focuses on mammalian models and the main strategies that are currently available, including transgenesis, viral vector gene delivery and the recently developed 'prion-like' models.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27158042</PMID>
<DateCreated><Year>2016</Year>
<Month>07</Month>
<Day>26</Day>
</DateCreated>
<DateRevised><Year>2016</Year>
<Month>12</Month>
<Day>19</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0035-3787</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>172</Volume>
<Issue>6-7</Issue>
<PubDate><MedlineDate>2016 Jun-Jul</MedlineDate>
</PubDate>
</JournalIssue>
<Title>Revue neurologique</Title>
<ISOAbbreviation>Rev. Neurol. (Paris)</ISOAbbreviation>
</Journal>
<ArticleTitle>Alpha-synuclein-based models of Parkinson's disease.</ArticleTitle>
<Pagination><MedlinePgn>371-8</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neurol.2016.04.003</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0035-3787(15)30038-2</ELocationID>
<Abstract><AbstractText>Parkinson's disease is a progressive neurodegenerative disorder mainly characterized by the loss of dopaminergic neurons from the substantia nigra pars compacta and the presence, in the affected brain regions, of protein inclusions called 'Lewy bodies'. Most cases are sporadic, but mutations in several genes, including SNCA, which encodes α-synuclein, are associated with disease development. A myriad of α-synuclein-based models for studying Parkinson's disease have been generated over the last two decades through different methodologies. Collectively, these models offer new opportunities to elucidate the mechanisms underlying the relentless progression of protein aggregation and neurodegeneration in Parkinson's. The present, non-exhaustive review focuses on mammalian models and the main strategies that are currently available, including transgenesis, viral vector gene delivery and the recently developed 'prion-like' models.</AbstractText>
<CopyrightInformation>Copyright © 2016 Elsevier Masson SAS. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dehay</LastName>
<ForeName>B</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Institut des maladies neurodégénératives, université de Bordeaux, UMR 5293, 33000 Bordeaux, France; CNRS, institut des maladies neurodégénératives, UMR 5293, 33000 Bordeaux, France. Electronic address: benjamin.dehay@u-bordeaux.fr.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fernagut</LastName>
<ForeName>P-O</ForeName>
<Initials>PO</Initials>
<AffiliationInfo><Affiliation>Institut des maladies neurodégénératives, université de Bordeaux, UMR 5293, 33000 Bordeaux, France; CNRS, institut des maladies neurodégénératives, UMR 5293, 33000 Bordeaux, France.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D016454">Review</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>05</Month>
<Day>02</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>France</Country>
<MedlineTA>Rev Neurol (Paris)</MedlineTA>
<NlmUniqueID>2984779R</NlmUniqueID>
<ISSNLinking>0035-3787</ISSNLinking>
</MedlineJournalInfo>
<CitationSubset>IM</CitationSubset>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alpha-synuclein</Keyword>
<Keyword MajorTopicYN="N">Animal models</Keyword>
<Keyword MajorTopicYN="N">Neurodegeneration</Keyword>
<Keyword MajorTopicYN="N">Parkinson</Keyword>
<Keyword MajorTopicYN="N">Synucleinopathy</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>11</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2016</Year>
<Month>04</Month>
<Day>04</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2016</Year>
<Month>04</Month>
<Day>04</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2016</Year>
<Month>5</Month>
<Day>10</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2016</Year>
<Month>5</Month>
<Day>10</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2016</Year>
<Month>5</Month>
<Day>10</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">27158042</ArticleId>
<ArticleId IdType="pii">S0035-3787(15)30038-2</ArticleId>
<ArticleId IdType="doi">10.1016/j.neurol.2016.04.003</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000138 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 000138 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonFranceV1 |flux= PubMed |étape= Corpus |type= RBID |clé= pubmed:27158042 |texte= Alpha-synuclein-based models of Parkinson's disease. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:27158042" \ | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \ | NlmPubMed2Wicri -a ParkinsonFranceV1
![]() | This area was generated with Dilib version V0.6.29. | ![]() |