Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease
Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease. We created a LRRK2 transgenic mouse model that recapitulates cardinal features of the disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dop...
Gespeichert in:
| Veröffentlicht in: | Nature neuroscience 2009-07, Vol.12 (7), p.826-828 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 828 |
|---|---|
| container_issue | 7 |
| container_start_page | 826 |
| container_title | Nature neuroscience |
| container_volume | 12 |
| creator | Li, Yanping Liu, Wencheng Oo, Tinmarla F Wang, Lei Tang, Yi Jackson-Lewis, Vernice Zhou, Chun Geghman, Kindiya Bogdanov, Mikhail Przedborski, Serge Beal, M Flint Burke, Robert E Li, Chenjian |
| description | Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease. We created a LRRK2 transgenic mouse model that recapitulates cardinal features of the disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projection. These mice provide a valid model of Parkinson's disease and are a resource for the investigation of pathogenesis and therapeutics. |
| doi_str_mv | 10.1038/nn.2349 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_67415245</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67415245</sourcerecordid><originalsourceid>FETCH-LOGICAL-p209t-b9faf706eebb612f6592c532014842882929256e0ce8c7c0ab6f77a348f3b4083</originalsourceid><addsrcrecordid>eNo1kEtLAzEYRYMgtlbxH0hWPhZT857MUotWsaIU3Tpk0i8SncmMSWbhv7dg5S7u5nDgXoROKJlTwvVVCHPGRbWHplQKVdCSqQk6TOmTEFJKXR2gCa0k4UTzKXp_GrMJGa_W60d2saZC0OUlvrle4BxNSB8QvMWdt4AjWDP4PLYmA7YmbnwwLXZg8hgh4d7hFxO_fEh9OE944xOYBEdo35k2wfGuZ-jt7vZ1cV-snpcPi-tVMTBS5aKpnHElUQBNoyhzSlbMSs4IFVowrVm1jVRALGhbWmIa5crScKEdb8R2yAyd_XmH2H-PkHLd-WShbU2Afky1KgWVTMgteLoDx6aDTT1E35n4U_8_wn8BrGNdlw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67415245</pqid></control><display><type>article</type><title>Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease</title><source>MEDLINE</source><source>Nature Journals Online</source><source>SpringerLink Journals - AutoHoldings</source><creator>Li, Yanping ; Liu, Wencheng ; Oo, Tinmarla F ; Wang, Lei ; Tang, Yi ; Jackson-Lewis, Vernice ; Zhou, Chun ; Geghman, Kindiya ; Bogdanov, Mikhail ; Przedborski, Serge ; Beal, M Flint ; Burke, Robert E ; Li, Chenjian</creator><creatorcontrib>Li, Yanping ; Liu, Wencheng ; Oo, Tinmarla F ; Wang, Lei ; Tang, Yi ; Jackson-Lewis, Vernice ; Zhou, Chun ; Geghman, Kindiya ; Bogdanov, Mikhail ; Przedborski, Serge ; Beal, M Flint ; Burke, Robert E ; Li, Chenjian</creatorcontrib><description>Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease. We created a LRRK2 transgenic mouse model that recapitulates cardinal features of the disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projection. These mice provide a valid model of Parkinson's disease and are a resource for the investigation of pathogenesis and therapeutics.</description><identifier>EISSN: 1546-1726</identifier><identifier>DOI: 10.1038/nn.2349</identifier><identifier>PMID: 19503083</identifier><language>eng</language><publisher>United States</publisher><subject>Age Factors ; Animals ; Antiparkinson Agents - therapeutic use ; Apomorphine - therapeutic use ; Brain - drug effects ; Brain - pathology ; Brain - physiopathology ; Chromosomes, Artificial, Bacterial ; Disease Models, Animal ; Dopamine - metabolism ; Dopamine Uptake Inhibitors - pharmacology ; Gene Transfer Techniques ; Humans ; Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 ; Levodopa - therapeutic use ; Mice ; Mice, Transgenic ; Movement Disorders - drug therapy ; Movement Disorders - genetics ; Mutation, Missense ; Neurons - pathology ; Neurons - physiology ; Nomifensine - pharmacology ; Parkinson Disease - genetics ; Parkinson Disease - pathology ; Parkinson Disease - physiopathology ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism</subject><ispartof>Nature neuroscience, 2009-07, Vol.12 (7), p.826-828</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19503083$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yanping</creatorcontrib><creatorcontrib>Liu, Wencheng</creatorcontrib><creatorcontrib>Oo, Tinmarla F</creatorcontrib><creatorcontrib>Wang, Lei</creatorcontrib><creatorcontrib>Tang, Yi</creatorcontrib><creatorcontrib>Jackson-Lewis, Vernice</creatorcontrib><creatorcontrib>Zhou, Chun</creatorcontrib><creatorcontrib>Geghman, Kindiya</creatorcontrib><creatorcontrib>Bogdanov, Mikhail</creatorcontrib><creatorcontrib>Przedborski, Serge</creatorcontrib><creatorcontrib>Beal, M Flint</creatorcontrib><creatorcontrib>Burke, Robert E</creatorcontrib><creatorcontrib>Li, Chenjian</creatorcontrib><title>Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease</title><title>Nature neuroscience</title><addtitle>Nat Neurosci</addtitle><description>Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease. We created a LRRK2 transgenic mouse model that recapitulates cardinal features of the disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projection. These mice provide a valid model of Parkinson's disease and are a resource for the investigation of pathogenesis and therapeutics.</description><subject>Age Factors</subject><subject>Animals</subject><subject>Antiparkinson Agents - therapeutic use</subject><subject>Apomorphine - therapeutic use</subject><subject>Brain - drug effects</subject><subject>Brain - pathology</subject><subject>Brain - physiopathology</subject><subject>Chromosomes, Artificial, Bacterial</subject><subject>Disease Models, Animal</subject><subject>Dopamine - metabolism</subject><subject>Dopamine Uptake Inhibitors - pharmacology</subject><subject>Gene Transfer Techniques</subject><subject>Humans</subject><subject>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</subject><subject>Levodopa - therapeutic use</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Movement Disorders - drug therapy</subject><subject>Movement Disorders - genetics</subject><subject>Mutation, Missense</subject><subject>Neurons - pathology</subject><subject>Neurons - physiology</subject><subject>Nomifensine - pharmacology</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson Disease - pathology</subject><subject>Parkinson Disease - physiopathology</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><issn>1546-1726</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kEtLAzEYRYMgtlbxH0hWPhZT857MUotWsaIU3Tpk0i8SncmMSWbhv7dg5S7u5nDgXoROKJlTwvVVCHPGRbWHplQKVdCSqQk6TOmTEFJKXR2gCa0k4UTzKXp_GrMJGa_W60d2saZC0OUlvrle4BxNSB8QvMWdt4AjWDP4PLYmA7YmbnwwLXZg8hgh4d7hFxO_fEh9OE944xOYBEdo35k2wfGuZ-jt7vZ1cV-snpcPi-tVMTBS5aKpnHElUQBNoyhzSlbMSs4IFVowrVm1jVRALGhbWmIa5crScKEdb8R2yAyd_XmH2H-PkHLd-WShbU2Afky1KgWVTMgteLoDx6aDTT1E35n4U_8_wn8BrGNdlw</recordid><startdate>200907</startdate><enddate>200907</enddate><creator>Li, Yanping</creator><creator>Liu, Wencheng</creator><creator>Oo, Tinmarla F</creator><creator>Wang, Lei</creator><creator>Tang, Yi</creator><creator>Jackson-Lewis, Vernice</creator><creator>Zhou, Chun</creator><creator>Geghman, Kindiya</creator><creator>Bogdanov, Mikhail</creator><creator>Przedborski, Serge</creator><creator>Beal, M Flint</creator><creator>Burke, Robert E</creator><creator>Li, Chenjian</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200907</creationdate><title>Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease</title><author>Li, Yanping ; Liu, Wencheng ; Oo, Tinmarla F ; Wang, Lei ; Tang, Yi ; Jackson-Lewis, Vernice ; Zhou, Chun ; Geghman, Kindiya ; Bogdanov, Mikhail ; Przedborski, Serge ; Beal, M Flint ; Burke, Robert E ; Li, Chenjian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p209t-b9faf706eebb612f6592c532014842882929256e0ce8c7c0ab6f77a348f3b4083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Age Factors</topic><topic>Animals</topic><topic>Antiparkinson Agents - therapeutic use</topic><topic>Apomorphine - therapeutic use</topic><topic>Brain - drug effects</topic><topic>Brain - pathology</topic><topic>Brain - physiopathology</topic><topic>Chromosomes, Artificial, Bacterial</topic><topic>Disease Models, Animal</topic><topic>Dopamine - metabolism</topic><topic>Dopamine Uptake Inhibitors - pharmacology</topic><topic>Gene Transfer Techniques</topic><topic>Humans</topic><topic>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</topic><topic>Levodopa - therapeutic use</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Movement Disorders - drug therapy</topic><topic>Movement Disorders - genetics</topic><topic>Mutation, Missense</topic><topic>Neurons - pathology</topic><topic>Neurons - physiology</topic><topic>Nomifensine - pharmacology</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson Disease - pathology</topic><topic>Parkinson Disease - physiopathology</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yanping</creatorcontrib><creatorcontrib>Liu, Wencheng</creatorcontrib><creatorcontrib>Oo, Tinmarla F</creatorcontrib><creatorcontrib>Wang, Lei</creatorcontrib><creatorcontrib>Tang, Yi</creatorcontrib><creatorcontrib>Jackson-Lewis, Vernice</creatorcontrib><creatorcontrib>Zhou, Chun</creatorcontrib><creatorcontrib>Geghman, Kindiya</creatorcontrib><creatorcontrib>Bogdanov, Mikhail</creatorcontrib><creatorcontrib>Przedborski, Serge</creatorcontrib><creatorcontrib>Beal, M Flint</creatorcontrib><creatorcontrib>Burke, Robert E</creatorcontrib><creatorcontrib>Li, Chenjian</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Nature neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yanping</au><au>Liu, Wencheng</au><au>Oo, Tinmarla F</au><au>Wang, Lei</au><au>Tang, Yi</au><au>Jackson-Lewis, Vernice</au><au>Zhou, Chun</au><au>Geghman, Kindiya</au><au>Bogdanov, Mikhail</au><au>Przedborski, Serge</au><au>Beal, M Flint</au><au>Burke, Robert E</au><au>Li, Chenjian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease</atitle><jtitle>Nature neuroscience</jtitle><addtitle>Nat Neurosci</addtitle><date>2009-07</date><risdate>2009</risdate><volume>12</volume><issue>7</issue><spage>826</spage><epage>828</epage><pages>826-828</pages><eissn>1546-1726</eissn><abstract>Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson's disease. We created a LRRK2 transgenic mouse model that recapitulates cardinal features of the disease: an age-dependent and levodopa-responsive slowness of movement associated with diminished dopamine release and axonal pathology of nigrostriatal dopaminergic projection. These mice provide a valid model of Parkinson's disease and are a resource for the investigation of pathogenesis and therapeutics.</abstract><cop>United States</cop><pmid>19503083</pmid><doi>10.1038/nn.2349</doi><tpages>3</tpages></addata></record> |
| fulltext | fulltext |
| identifier | EISSN: 1546-1726 |
| ispartof | Nature neuroscience, 2009-07, Vol.12 (7), p.826-828 |
| issn | 1546-1726 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67415245 |
| source | MEDLINE; Nature Journals Online; SpringerLink Journals - AutoHoldings |
| subjects | Age Factors Animals Antiparkinson Agents - therapeutic use Apomorphine - therapeutic use Brain - drug effects Brain - pathology Brain - physiopathology Chromosomes, Artificial, Bacterial Disease Models, Animal Dopamine - metabolism Dopamine Uptake Inhibitors - pharmacology Gene Transfer Techniques Humans Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 Levodopa - therapeutic use Mice Mice, Transgenic Movement Disorders - drug therapy Movement Disorders - genetics Mutation, Missense Neurons - pathology Neurons - physiology Nomifensine - pharmacology Parkinson Disease - genetics Parkinson Disease - pathology Parkinson Disease - physiopathology Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism |
| title | Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T08%3A48%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Mutant%20LRRK2(R1441G)%20BAC%20transgenic%20mice%20recapitulate%20cardinal%20features%20of%20Parkinson's%20disease&rft.jtitle=Nature%20neuroscience&rft.au=Li,%20Yanping&rft.date=2009-07&rft.volume=12&rft.issue=7&rft.spage=826&rft.epage=828&rft.pages=826-828&rft.eissn=1546-1726&rft_id=info:doi/10.1038/nn.2349&rft_dat=%3Cproquest_pubme%3E67415245%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67415245&rft_id=info:pmid/19503083&rfr_iscdi=true |