LRRK2 Parkinson’s disease: from animal models to cellular mechanisms
Identifieur interne : 000091 ( Main/Corpus ); précédent : 000090; suivant : 000092LRRK2 Parkinson’s disease: from animal models to cellular mechanisms
Auteurs : Chin-Hsien Lin ; Pei-I Tsai ; Ruey-Meei Wu ; Cheng-Ting ChienSource :
- Reviews in the Neurosciences [ 0334-1763 ] ; 2011-08-01.
Abstract
Mutations in the gene encoding leucine-rich repeat kinase 2 (LRRK2) play a major role in the development of Parkinson’s disease. The most frequently defined mutations of LRRK2 are located in the central catalytic region of the LRRK2 protein, suggesting that dysregulations of its enzymatic activities contribute to PD pathogenesis. Herein, we review recent progress in research concerning how LRRK2 mutations affect cellular pathways and lead to neuronal degeneration. We also summarize recent evidence revealing the endogenous function of LRRK2 protein within cells. These concepts can be used to further understand disease pathophysiology and serve as a platform to develop therapeutic strategies for the treatment of Parkinson’s disease.
Url:
DOI: 10.1515/rns.2011.036
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The most frequently defined mutations of <italic>LRRK2</italic> are located in the central catalytic region of the LRRK2 protein, suggesting that dysregulations of its enzymatic activities contribute to PD pathogenesis. Herein, we review recent progress in research concerning how <italic>LRRK2</italic> mutations affect cellular pathways and lead to neuronal degeneration. We also summarize recent evidence revealing the endogenous function of LRRK2 protein within cells. These concepts can be used to further understand disease pathophysiology and serve as a platform to develop therapeutic strategies for the treatment of Parkinson’s disease.</p></abstract><kwd-group><title>Keywords</title><kwd>animal models</kwd><x>, </x><kwd><italic>LRRK2</italic></kwd><x>, </x><kwd>Parkinson’s disease</kwd></kwd-group><counts><fig-count count="2"></fig-count><table-count count="1"></table-count><ref-count count="56"></ref-count></counts></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>LRRK2 Parkinson’s disease: from animal models to cellular mechanisms</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>LRRK2 Parkinson’s disease: from animal models to cellular mechanisms</title></titleInfo><name type="personal"><namePart type="given">Chin-Hsien</namePart><namePart type="family">Lin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pei-I</namePart><namePart type="family">Tsai</namePart><affiliation>Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ruey-Meei</namePart><namePart type="family">Wu</namePart><affiliation>Department of Neurology, National Taiwan University Hospital, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cheng-Ting</namePart><namePart type="family">Chien</namePart><affiliation>Institute of Molecular Biology, Academia Sinica, Taipei, Taiwan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Walter de Gruyter</publisher><dateIssued encoding="w3cdtf">2011-08-01</dateIssued><dateCreated encoding="w3cdtf">2011-06-17</dateCreated><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">1</extent><extent unit="references">56</extent></physicalDescription><abstract lang="en">Mutations in the gene encoding leucine-rich repeat kinase 2 (LRRK2) play a major role in the development of Parkinson’s disease. The most frequently defined mutations of LRRK2 are located in the central catalytic region of the LRRK2 protein, suggesting that dysregulations of its enzymatic activities contribute to PD pathogenesis. Herein, we review recent progress in research concerning how LRRK2 mutations affect cellular pathways and lead to neuronal degeneration. We also summarize recent evidence revealing the endogenous function of LRRK2 protein within cells. These concepts can be used to further understand disease pathophysiology and serve as a platform to develop therapeutic strategies for the treatment of Parkinson’s disease.</abstract><note type="author-notes">Corresponding author</note><subject><genre>Keywords</genre><topic>animal models</topic><topic>LRRK2</topic><topic>Parkinson’s disease</topic></subject><relatedItem type="host"><titleInfo><title>Reviews in the Neurosciences</title></titleInfo><titleInfo type="abbreviated"><title>Reviews in the Neurosciences</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0334-1763</identifier><identifier type="eISSN">2191-0200</identifier><identifier type="PublisherID">revneuro</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>411</start><end>418</end></extent></part></relatedItem><relatedItem type="reviewOf"><genre>pdf</genre><identifier type="pdf">rns.2011.036.pdf</identifier></relatedItem><identifier type="istex">974093E1AC1BC521DFE32518612AF37A2D9B8BB6</identifier><identifier type="DOI">10.1515/rns.2011.036</identifier><identifier type="ArticleID">rns.2011.036</identifier><identifier type="Related-article-Href">rns.2011.036.pdf</identifier><accessCondition type="use and reproduction" contentType="copyright">©2011 by Walter de Gruyter Berlin Boston</accessCondition><recordInfo><recordContentSource>De Gruyter</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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