LRRK2 Kinase Inhibition as a Therapeutic Strategy for Parkinson's Disease, Where Do We Stand?
Identifieur interne : 000216 ( PubMed/Corpus ); précédent : 000215; suivant : 000217LRRK2 Kinase Inhibition as a Therapeutic Strategy for Parkinson's Disease, Where Do We Stand?
Auteurs : Jean-Marc Taymans ; Elisa GreggioSource :
- Current neuropharmacology [ 1875-6190 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (therapeutic use), Drug Evaluation, Preclinical, Enzyme Inhibitors (therapeutic use), Humans, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (genetics), Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (metabolism), Parkinson Disease (genetics), Parkinson Disease (therapy).
- MESH :
- chemical , genetics : Leucine-Rich Repeat Serine-Threonine Protein Kinase-2.
- chemical , metabolism : Leucine-Rich Repeat Serine-Threonine Protein Kinase-2.
- chemical , therapeutic use : Antiparkinson Agents, Enzyme Inhibitors.
- genetics : Parkinson Disease.
- therapy : Parkinson Disease.
- Animals, Drug Evaluation, Preclinical, Humans.
Abstract
One of the most promising therapeutic targets for potential disease-modifying treatment of Parkinson's disease (PD) is leucine-rich repeat kinase 2 (LRRK2). Specifically, targeting LRRK2's kinase function has generated a lot of interest from both industry and academia. This work has yielded several published studies showing the feasibility of developing potent, selective and brain permeable LRRK2 kinase inhibitors. The availability of these experimental drugs is contributing to filling in the gaps in our knowledge on the safety and efficacy of LRRK2 kinase inhibition. Recent studies of LRRK2 kinase inhibition in preclinical models point to potential undesired effects in peripheral tissues such as lung and kidney. Also, while strategies are now emerging to measure target engagement of LRRK2 inhibitors, there remains an important need to expand efficacy studies in preclinical models of progressive PD. Future work in the LRRK2 inhibition field must therefore be directed towards developing molecules and treatment regimens which demonstrate efficacy in mammalian models of disease in conditions where safety liabilities are reduced to a minimum.
PubMed: 26517051
Links to Exploration step
pubmed:26517051Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">LRRK2 Kinase Inhibition as a Therapeutic Strategy for Parkinson's Disease, Where Do We Stand?</title><author><name sortKey="Taymans, Jean Marc" sort="Taymans, Jean Marc" uniqKey="Taymans J" first="Jean-Marc" last="Taymans">Jean-Marc Taymans</name><affiliation><nlm:affiliation>Jean-Pierre Aubert Research Center, UMR-S1172,rue Polonovski - 1 place de Verdun, 59045 Lille, France. jean-marc.taymans@inserm.fr.</nlm:affiliation></affiliation></author><author><name sortKey="Greggio, Elisa" sort="Greggio, Elisa" uniqKey="Greggio E" first="Elisa" last="Greggio">Elisa Greggio</name><affiliation><nlm:affiliation>Department of Biology, University of Padova, 35131, Padova, Italy. elisa.greggio@unipd.it.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26517051</idno><idno type="pmid">26517051</idno><idno type="wicri:Area/PubMed/Corpus">000216</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000216</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">LRRK2 Kinase Inhibition as a Therapeutic Strategy for Parkinson's Disease, Where Do We Stand?</title><author><name sortKey="Taymans, Jean Marc" sort="Taymans, Jean Marc" uniqKey="Taymans J" first="Jean-Marc" last="Taymans">Jean-Marc Taymans</name><affiliation><nlm:affiliation>Jean-Pierre Aubert Research Center, UMR-S1172,rue Polonovski - 1 place de Verdun, 59045 Lille, France. jean-marc.taymans@inserm.fr.</nlm:affiliation></affiliation></author><author><name sortKey="Greggio, Elisa" sort="Greggio, Elisa" uniqKey="Greggio E" first="Elisa" last="Greggio">Elisa Greggio</name><affiliation><nlm:affiliation>Department of Biology, University of Padova, 35131, Padova, Italy. elisa.greggio@unipd.it.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Current neuropharmacology</title><idno type="eISSN">1875-6190</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (therapeutic use)</term><term>Drug Evaluation, Preclinical</term><term>Enzyme Inhibitors (therapeutic use)</term><term>Humans</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (genetics)</term><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 (metabolism)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (therapy)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Evaluation, Preclinical</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">One of the most promising therapeutic targets for potential disease-modifying treatment of Parkinson's disease (PD) is leucine-rich repeat kinase 2 (LRRK2). Specifically, targeting LRRK2's kinase function has generated a lot of interest from both industry and academia. This work has yielded several published studies showing the feasibility of developing potent, selective and brain permeable LRRK2 kinase inhibitors. The availability of these experimental drugs is contributing to filling in the gaps in our knowledge on the safety and efficacy of LRRK2 kinase inhibition. Recent studies of LRRK2 kinase inhibition in preclinical models point to potential undesired effects in peripheral tissues such as lung and kidney. Also, while strategies are now emerging to measure target engagement of LRRK2 inhibitors, there remains an important need to expand efficacy studies in preclinical models of progressive PD. Future work in the LRRK2 inhibition field must therefore be directed towards developing molecules and treatment regimens which demonstrate efficacy in mammalian models of disease in conditions where safety liabilities are reduced to a minimum.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26517051</PMID><DateCreated><Year>2016</Year><Month>03</Month><Day>08</Day></DateCreated><DateCompleted><Year>2016</Year><Month>12</Month><Day>13</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>30</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1875-6190</ISSN><JournalIssue CitedMedium="Internet"><Volume>14</Volume><Issue>3</Issue><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Current neuropharmacology</Title><ISOAbbreviation>Curr Neuropharmacol</ISOAbbreviation></Journal><ArticleTitle>LRRK2 Kinase Inhibition as a Therapeutic Strategy for Parkinson's Disease, Where Do We Stand?</ArticleTitle><Pagination><MedlinePgn>214-25</MedlinePgn></Pagination><Abstract><AbstractText>One of the most promising therapeutic targets for potential disease-modifying treatment of Parkinson's disease (PD) is leucine-rich repeat kinase 2 (LRRK2). Specifically, targeting LRRK2's kinase function has generated a lot of interest from both industry and academia. This work has yielded several published studies showing the feasibility of developing potent, selective and brain permeable LRRK2 kinase inhibitors. The availability of these experimental drugs is contributing to filling in the gaps in our knowledge on the safety and efficacy of LRRK2 kinase inhibition. Recent studies of LRRK2 kinase inhibition in preclinical models point to potential undesired effects in peripheral tissues such as lung and kidney. Also, while strategies are now emerging to measure target engagement of LRRK2 inhibitors, there remains an important need to expand efficacy studies in preclinical models of progressive PD. Future work in the LRRK2 inhibition field must therefore be directed towards developing molecules and treatment regimens which demonstrate efficacy in mammalian models of disease in conditions where safety liabilities are reduced to a minimum.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Taymans</LastName><ForeName>Jean-Marc</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Jean-Pierre Aubert Research Center, UMR-S1172,rue Polonovski - 1 place de Verdun, 59045 Lille, France. jean-marc.taymans@inserm.fr.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Greggio</LastName><ForeName>Elisa</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Biology, University of Padova, 35131, Padova, Italy. elisa.greggio@unipd.it.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United Arab Emirates</Country><MedlineTA>Curr Neuropharmacol</MedlineTA><NlmUniqueID>101157239</NlmUniqueID><ISSNLinking>1570-159X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000071158">Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 2009 Dec;41(12):1308-12</RefSource><PMID 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MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004353" MajorTopicYN="N">Drug Evaluation, Preclinical</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004791" MajorTopicYN="N">Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000071158" MajorTopicYN="N">Leucine-Rich Repeat Serine-Threonine Protein Kinase-2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4857626 [Available on 10/01/16]</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>04</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>06</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>06</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26517051</ArticleId><ArticleId IdType="pii">CN-EPUB-71450</ArticleId><ArticleId IdType="pmc">PMC4857626</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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