Emerging drugs for levodopa-induced dyskinesia.
Identifieur interne : 000742 ( PubMed/Checkpoint ); précédent : 000741; suivant : 000743Emerging drugs for levodopa-induced dyskinesia.
Auteurs : Amaal Al Dakheel [Canada] ; Isabelle Beaulieu-Boire ; Susan H. FoxSource :
- Expert opinion on emerging drugs [ 1744-7623 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Antiparkinson Agents (adverse effects), Antiparkinson Agents (therapeutic use), Basal Ganglia (pathology), Drug Design, Dyskinesia, Drug-Induced (drug therapy), Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (prevention & control), Humans, Levodopa (adverse effects), Levodopa (therapeutic use), Parkinson Disease (drug therapy), Randomized Controlled Trials as Topic, Receptors, Dopamine (drug effects), Receptors, Dopamine (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , drug effects : Receptors, Dopamine.
- chemical , metabolism : Receptors, Dopamine.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- drug effects : Signal Transduction.
- drug therapy : Dyskinesia, Drug-Induced, Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- pathology : Basal Ganglia.
- prevention & control : Dyskinesia, Drug-Induced.
- Animals, Drug Design, Humans, Randomized Controlled Trials as Topic.
Abstract
Levodopa continues to be the main symptomatic therapy for clinical features of Parkinson's disease. However, prolonged use leads to motor complications, including levodopa-induced dyskinesia (LID). This has debilitating impact on the patients and is a significant challenge for the treating physician. There are currently limited pharmacological options for reducing established LID without causing side effects. Drugs to prevent or delay LID are also an increasing part of the strategy to manage LID, but have yet to show promise. Agents that allow levodopa to be used effectively, without inducing LID, are the goal of current research strategies.
DOI: 10.1517/14728214.2014.955014
PubMed: 25146568
Affiliations:
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Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network , Toronto, ON </wicri:regionArea><wicri:noRegion>ON </wicri:noRegion></affiliation></author><author><name sortKey="Beaulieu Boire, Isabelle" sort="Beaulieu Boire, Isabelle" uniqKey="Beaulieu Boire I" first="Isabelle" last="Beaulieu-Boire">Isabelle Beaulieu-Boire</name></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. 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Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network , Toronto, ON , Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network , Toronto, ON </wicri:regionArea><wicri:noRegion>ON </wicri:noRegion></affiliation></author><author><name sortKey="Beaulieu Boire, Isabelle" sort="Beaulieu Boire, Isabelle" uniqKey="Beaulieu Boire I" first="Isabelle" last="Beaulieu-Boire">Isabelle Beaulieu-Boire</name></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name></author></analytic><series><title level="j">Expert opinion on emerging drugs</title><idno type="eISSN">1744-7623</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Basal Ganglia (pathology)</term><term>Drug Design</term><term>Dyskinesia, Drug-Induced (drug therapy)</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Dyskinesia, Drug-Induced (prevention & control)</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Levodopa (therapeutic use)</term><term>Parkinson Disease (drug therapy)</term><term>Randomized Controlled Trials as Topic</term><term>Receptors, Dopamine (drug effects)</term><term>Receptors, Dopamine (metabolism)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Design</term><term>Humans</term><term>Randomized Controlled Trials as Topic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Levodopa continues to be the main symptomatic therapy for clinical features of Parkinson's disease. However, prolonged use leads to motor complications, including levodopa-induced dyskinesia (LID). This has debilitating impact on the patients and is a significant challenge for the treating physician. There are currently limited pharmacological options for reducing established LID without causing side effects. Drugs to prevent or delay LID are also an increasing part of the strategy to manage LID, but have yet to show promise. Agents that allow levodopa to be used effectively, without inducing LID, are the goal of current research strategies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25146568</PMID><DateCreated><Year>2014</Year><Month>08</Month><Day>29</Day></DateCreated><DateCompleted><Year>2015</Year><Month>03</Month><Day>30</Day></DateCompleted><DateRevised><Year>2014</Year><Month>08</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1744-7623</ISSN><JournalIssue CitedMedium="Internet"><Volume>19</Volume><Issue>3</Issue><PubDate><Year>2014</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Expert opinion on emerging drugs</Title><ISOAbbreviation>Expert Opin Emerg Drugs</ISOAbbreviation></Journal><ArticleTitle>Emerging drugs for levodopa-induced dyskinesia.</ArticleTitle><Pagination><MedlinePgn>415-29</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1517/14728214.2014.955014</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">Levodopa continues to be the main symptomatic therapy for clinical features of Parkinson's disease. However, prolonged use leads to motor complications, including levodopa-induced dyskinesia (LID). This has debilitating impact on the patients and is a significant challenge for the treating physician. There are currently limited pharmacological options for reducing established LID without causing side effects. Drugs to prevent or delay LID are also an increasing part of the strategy to manage LID, but have yet to show promise. Agents that allow levodopa to be used effectively, without inducing LID, are the goal of current research strategies.</AbstractText><AbstractText Label="AREAS COVERED" NlmCategory="METHODS">LID occurs due to significant modifications in the basal ganglia circuitry, probably related to the chronic, pulsatile stimulation of striatal dopaminergic receptors by levodopa, as well as altered non-dopaminergic neurotransmitter system signaling pathways. Novel treatments that either result in continuous dopaminergic receptor stimulation, levodopa 'sparing strategies' or non-dopaminergic targets, including glutamatergic, serotonergic, adenosine, adrenergic and cholinergic neurotransmission are thus the main treatment options and the focus of this manuscript. Randomized controlled trials in progress (ClinicalTrials.org) or recently published articles are included.</AbstractText><AbstractText Label="EXPERT OPINION" NlmCategory="CONCLUSIONS">The success of future therapeutic approaches will depend on the potential success of translational research.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Al Dakheel</LastName><ForeName>Amaal</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, University Health Network , Toronto, ON , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Beaulieu-Boire</LastName><ForeName>Isabelle</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Fox</LastName><ForeName>Susan H</ForeName><Initials>SH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>08</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Opin Emerg Drugs</MedlineTA><NlmUniqueID>101135662</NlmUniqueID><ISSNLinking>1472-8214</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011954">Receptors, Dopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001479" MajorTopicYN="N">Basal Ganglia</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015195" MajorTopicYN="N">Drug Design</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016032" MajorTopicYN="N">Randomized Controlled Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011954" MajorTopicYN="N">Receptors, Dopamine</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">dopaminergic/non-dopaminergic systems</Keyword><Keyword MajorTopicYN="N">levodopa-induced dyskinesia</Keyword><Keyword MajorTopicYN="N">pharmacotherapy</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>8</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>8</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>3</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25146568</ArticleId><ArticleId IdType="doi">10.1517/14728214.2014.955014</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Beaulieu Boire, Isabelle" sort="Beaulieu Boire, Isabelle" uniqKey="Beaulieu Boire I" first="Isabelle" last="Beaulieu-Boire">Isabelle Beaulieu-Boire</name><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name></noCountry><country name="Canada"><noRegion><name sortKey="Al Dakheel, Amaal" sort="Al Dakheel, Amaal" uniqKey="Al Dakheel A" first="Amaal" last="Al Dakheel">Amaal Al Dakheel</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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