Genetic LRRK2 models of Parkinson's disease: Dissecting the pathogenic pathway and exploring clinical applications
Identifieur interne : 000308 ( Main/Exploration ); précédent : 000307; suivant : 000309Genetic LRRK2 models of Parkinson's disease: Dissecting the pathogenic pathway and exploring clinical applications
Auteurs : Zhenyu Yue [États-Unis] ; M. Lenard Lachenmayer [États-Unis, Allemagne]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-07.
English descriptors
- KwdEn :
Abstract
Dominantly inherited mutations in leucine‐rich repeat kinase 2 are the most common cause of familial Parkinson's disease. Understanding leucine‐rich repeat kinase 2 biology and pathophysiology is central to the elucidation of Parkinson's disease etiology and development of disease intervention. Recently, a number of genetic mouse models of leucine‐rich repeat kinase 2 have been reported utilizing different genetic approaches. Some similarities in Parkinson's disease‐related pathology emerge in these genetic models despite lack of substantial neuropathology and clinical syndromes of Parkinson's disease. The systematic characterization of these models has begun to shed light on leucine‐rich repeat kinase 2 biology and pathophysiology and is expected to offer the identification and validation of drug targets. In this review, we summarize the progress of genetic leucine‐rich repeat kinase 2 mouse models and discuss their utility in understanding much needed knowledge regarding early‐stage (presymptomatic) disease progression, identifying drug targets, and exploring the potential to aid compound screening focused on inhibitors of kinase activity of leucine‐rich repeat kinase 2. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23737
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Genetic LRRK2 models of Parkinson's disease: Dissecting the pathogenic pathway and exploring clinical applications</title>
<author><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name>
</author>
<author><name sortKey="Lachenmayer, M Lenard" sort="Lachenmayer, M Lenard" uniqKey="Lachenmayer M" first="M. Lenard" last="Lachenmayer">M. Lenard Lachenmayer</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:D0208C54ACF5F031456CF2987216364E1B1158E5</idno>
<date when="2011" year="2011">2011</date>
<idno type="doi">10.1002/mds.23737</idno>
<idno type="url">https://api.istex.fr/document/D0208C54ACF5F031456CF2987216364E1B1158E5/fulltext/pdf</idno>
<idno type="wicri:Area/Main/Corpus">000E36</idno>
<idno type="wicri:Area/Main/Curation">000C69</idno>
<idno type="wicri:Area/Main/Exploration">000308</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Genetic LRRK2 models of Parkinson's disease: Dissecting the pathogenic pathway and exploring clinical applications</title>
<author><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York</wicri:regionArea>
<placeName><region type="state">État de New York</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lachenmayer, M Lenard" sort="Lachenmayer, M Lenard" uniqKey="Lachenmayer M" first="M. Lenard" last="Lachenmayer">M. Lenard Lachenmayer</name>
<affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York</wicri:regionArea>
<placeName><region type="state">État de New York</region>
</placeName>
</affiliation>
<affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Bonn, Bonn</wicri:regionArea>
<placeName><region type="land" nuts="1">Rhénanie-du-Nord-Westphalie</region>
<region type="district" nuts="2">District de Cologne</region>
<settlement type="city">Bonn</settlement>
</placeName>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Movement Disorders</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2011-07">2011-07</date>
<biblScope unit="volume">26</biblScope>
<biblScope unit="issue">8</biblScope>
<biblScope unit="page" from="1386">1386</biblScope>
<biblScope unit="page" to="1397">1397</biblScope>
</imprint>
<idno type="ISSN">0885-3185</idno>
</series>
<idno type="istex">D0208C54ACF5F031456CF2987216364E1B1158E5</idno>
<idno type="DOI">10.1002/mds.23737</idno>
<idno type="ArticleID">MDS23737</idno>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>G2019S</term>
<term>Parkinson's disease</term>
<term>genetic mouse models</term>
<term>kinase inhibitors</term>
<term>leucine‐rich repeat kinase 2</term>
</keywords>
</textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Dominantly inherited mutations in leucine‐rich repeat kinase 2 are the most common cause of familial Parkinson's disease. Understanding leucine‐rich repeat kinase 2 biology and pathophysiology is central to the elucidation of Parkinson's disease etiology and development of disease intervention. Recently, a number of genetic mouse models of leucine‐rich repeat kinase 2 have been reported utilizing different genetic approaches. Some similarities in Parkinson's disease‐related pathology emerge in these genetic models despite lack of substantial neuropathology and clinical syndromes of Parkinson's disease. The systematic characterization of these models has begun to shed light on leucine‐rich repeat kinase 2 biology and pathophysiology and is expected to offer the identification and validation of drug targets. In this review, we summarize the progress of genetic leucine‐rich repeat kinase 2 mouse models and discuss their utility in understanding much needed knowledge regarding early‐stage (presymptomatic) disease progression, identifying drug targets, and exploring the potential to aid compound screening focused on inhibitors of kinase activity of leucine‐rich repeat kinase 2. © 2011 Movement Disorder Society</div>
</front>
</TEI>
<affiliations><list><country><li>Allemagne</li>
<li>États-Unis</li>
</country>
<region><li>District de Cologne</li>
<li>Rhénanie-du-Nord-Westphalie</li>
<li>État de New York</li>
</region>
<settlement><li>Bonn</li>
</settlement>
</list>
<tree><country name="États-Unis"><region name="État de New York"><name sortKey="Yue, Zhenyu" sort="Yue, Zhenyu" uniqKey="Yue Z" first="Zhenyu" last="Yue">Zhenyu Yue</name>
</region>
<name sortKey="Lachenmayer, M Lenard" sort="Lachenmayer, M Lenard" uniqKey="Lachenmayer M" first="M. Lenard" last="Lachenmayer">M. Lenard Lachenmayer</name>
</country>
<country name="Allemagne"><region name="Rhénanie-du-Nord-Westphalie"><name sortKey="Lachenmayer, M Lenard" sort="Lachenmayer, M Lenard" uniqKey="Lachenmayer M" first="M. Lenard" last="Lachenmayer">M. Lenard Lachenmayer</name>
</region>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000308 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000308 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonV1 |flux= Main |étape= Exploration |type= RBID |clé= ISTEX:D0208C54ACF5F031456CF2987216364E1B1158E5 |texte= Genetic LRRK2 models of Parkinson's disease: Dissecting the pathogenic pathway and exploring clinical applications }}
This area was generated with Dilib version V0.6.23. |