Ten years and counting: moving leucine-rich repeat kinase 2 inhibitors to the clinic.
Identifieur interne : 000339 ( PubMed/Corpus ); précédent : 000338; suivant : 000340Ten years and counting: moving leucine-rich repeat kinase 2 inhibitors to the clinic.
Auteurs : Andrew B. WestSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.
English descriptors
- KwdEn :
- MESH :
- chemical , antagonists & inhibitors : Protein-Serine-Threonine Kinases.
- chemical , genetics : Protein-Serine-Threonine Kinases.
- chemical , metabolism : Protein-Serine-Threonine Kinases.
- chemical , therapeutic use : Neuroprotective Agents.
- drug therapy : Parkinson Disease.
- genetics : Mutation, Parkinson Disease.
- Animals, Humans.
Abstract
The burden that Parkinson's disease (PD) exacts on the population continues to increase year after year. Though refinement of symptomatic treatments continues at a reasonable pace, no accepted therapies are available to slow or prevent disease progression. The leucine-rich repeat kinase 2 (LRRK2) gene was identified in PD genetic studies and offers new hope for novel therapeutic approaches. The evidence linking LRRK2 kinase activity to PD susceptibility is presented, as well as seminal discoveries relevant to the prosecution of LRRK2 kinase inhibition. Finally, suggestions are made for predictive preclinical modeling and successful first-in-human trials.
DOI: 10.1002/mds.26075
PubMed: 25448543
Links to Exploration step
pubmed:25448543Le document en format XML
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West</name><affiliation><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25448543</idno><idno type="pmid">25448543</idno><idno type="doi">10.1002/mds.26075</idno><idno type="wicri:Area/PubMed/Corpus">000339</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ten years and counting: moving leucine-rich repeat kinase 2 inhibitors to the clinic.</title><author><name sortKey="West, Andrew B" sort="West, Andrew B" uniqKey="West A" first="Andrew B" last="West">Andrew B. West</name><affiliation><nlm:affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Humans</term><term>Mutation (genetics)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (genetics)</term><term>Protein-Serine-Threonine Kinases (antagonists & inhibitors)</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Protein-Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The burden that Parkinson's disease (PD) exacts on the population continues to increase year after year. Though refinement of symptomatic treatments continues at a reasonable pace, no accepted therapies are available to slow or prevent disease progression. The leucine-rich repeat kinase 2 (LRRK2) gene was identified in PD genetic studies and offers new hope for novel therapeutic approaches. The evidence linking LRRK2 kinase activity to PD susceptibility is presented, as well as seminal discoveries relevant to the prosecution of LRRK2 kinase inhibition. Finally, suggestions are made for predictive preclinical modeling and successful first-in-human trials.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">25448543</PMID><DateCreated><Year>2015</Year><Month>02</Month><Day>04</Day></DateCreated><DateCompleted><Year>2015</Year><Month>10</Month><Day>22</Day></DateCompleted><DateRevised><Year>2015</Year><Month>03</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>30</Volume><Issue>2</Issue><PubDate><Year>2015</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Ten years and counting: moving leucine-rich repeat kinase 2 inhibitors to the clinic.</ArticleTitle><Pagination><MedlinePgn>180-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26075</ELocationID><Abstract><AbstractText>The burden that Parkinson's disease (PD) exacts on the population continues to increase year after year. Though refinement of symptomatic treatments continues at a reasonable pace, no accepted therapies are available to slow or prevent disease progression. The leucine-rich repeat kinase 2 (LRRK2) gene was identified in PD genetic studies and offers new hope for novel therapeutic approaches. The evidence linking LRRK2 kinase activity to PD susceptibility is presented, as well as seminal discoveries relevant to the prosecution of LRRK2 kinase inhibition. Finally, suggestions are made for predictive preclinical modeling and successful first-in-human trials.</AbstractText><CopyrightInformation>© 2014 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>West</LastName><ForeName>Andrew B</ForeName><Initials>AB</Initials><AffiliationInfo><Affiliation>Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 NS064934</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01NS064934</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U18 NS082132</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United 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protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 Feb 15;21(4):890-9</RefSource><PMID Version="1">22080837</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2012 Feb 1;32(5):1602-11</RefSource><PMID Version="1">22302802</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS Genet. 2012;8(3):e1002548</RefSource><PMID Version="1">22438815</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Drug Discov Today. 2012 May;17(9-10):419-24</RefSource><PMID Version="1">22227532</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 2012 Jun 1;21(11):2420-31</RefSource><PMID 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