Genetic LRRK2 Models of Parkinson's Disease: Dissecting the Pathogenic Pathway and Exploring Clinical Applications
Identifieur interne : 001885 ( Main/Exploration ); précédent : 001884; suivant : 001886Genetic 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.
Descripteurs français
- Pascal (Inist)
English descriptors
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.
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Lenard Lachenmayer</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurology and Neuroscience, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation><affiliation wicri:level="3"><inist:fA14 i1="02"><s1>Department of Neurology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>2 aut.</sZ></inist:fA14><country>Allemagne</country><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><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal model</term><term>Kinase</term><term>Leucine</term><term>Nervous system diseases</term><term>Parkinson disease</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Modèle animal</term><term>Leucine</term><term>Kinase</term></keywords></textClass></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.</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="Zhenyu Yue" sort="Zhenyu Yue" uniqKey="Zhenyu Yue" last="Zhenyu 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)
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