Mechanisms compensating for dopamine loss in early Parkinson disease.
Identifieur interne : 000E31 ( PubMed/Checkpoint ); précédent : 000E30; suivant : 000E32Mechanisms compensating for dopamine loss in early Parkinson disease.
Auteurs : Jonathan Brotchie [Canada] ; Cheryl Fitzer-AttasSource :
- Neurology [ 1526-632X ] ; 2009.
English descriptors
- KwdEn :
- Antiparkinson Agents (therapeutic use), Corpus Striatum (physiopathology), Disease Progression, Dopamine (metabolism), Globus Pallidus (physiopathology), Humans, Indans (therapeutic use), Levodopa (therapeutic use), Neural Pathways, Neurons (metabolism), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (physiopathology).
- MESH :
- chemical , metabolism : Dopamine.
- chemical , therapeutic use : Antiparkinson Agents, Indans, Levodopa.
- drug therapy : Parkinson Disease.
- metabolism : Neurons, Parkinson Disease.
- physiopathology : Corpus Striatum, Globus Pallidus, Parkinson Disease.
- Disease Progression, Humans, Neural Pathways.
Abstract
Parkinson disease (PD) is a disorder with a substantive period before the emergence of motor symptoms, during which significant dopaminergic neuronal loss is counterbalanced by endogenous compensatory mechanisms. Many potential compensatory mechanisms have now been proposed; these are both dopaminergic, focused on enhancing effects or exposure to existing dopamine, and nondopaminergic, being focused on reducing activity of the indirect striatal output pathway. Compensatory mechanisms can potentially postpone and reduce the severity of parkinsonian symptoms, and contribute to the benefit provided by a symptomatic therapy, thus offering targets for novel therapeutics. However, enhancement of certain compensatory mechanisms may produce problems when subsequent therapies are initiated, e.g., the development of motor complications with levodopa. Supporting endogenous compensatory mechanisms, to delay or reverse apparent disease progression, is a novel and attractive "disease-modifying" approach to PD. Such actions may contribute to the apparent disease-modifying benefit of initiating early treatment with levodopa or rasagiline, as suggested by the ELLDOPA and TEMPO studies.
DOI: 10.1212/WNL.0b013e318198e0e9
PubMed: 19221312
Affiliations:
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pubmed:19221312Le document en format XML
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Many potential compensatory mechanisms have now been proposed; these are both dopaminergic, focused on enhancing effects or exposure to existing dopamine, and nondopaminergic, being focused on reducing activity of the indirect striatal output pathway. Compensatory mechanisms can potentially postpone and reduce the severity of parkinsonian symptoms, and contribute to the benefit provided by a symptomatic therapy, thus offering targets for novel therapeutics. However, enhancement of certain compensatory mechanisms may produce problems when subsequent therapies are initiated, e.g., the development of motor complications with levodopa. Supporting endogenous compensatory mechanisms, to delay or reverse apparent disease progression, is a novel and attractive "disease-modifying" approach to PD. Such actions may contribute to the apparent disease-modifying benefit of initiating early treatment with levodopa or rasagiline, as suggested by the ELLDOPA and TEMPO studies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19221312</PMID><DateCreated><Year>2009</Year><Month>02</Month><Day>17</Day></DateCreated><DateCompleted><Year>2009</Year><Month>03</Month><Day>12</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1526-632X</ISSN><JournalIssue CitedMedium="Internet"><Volume>72</Volume><Issue>7 Suppl</Issue><PubDate><Year>2009</Year><Month>Feb</Month><Day>17</Day></PubDate></JournalIssue><Title>Neurology</Title><ISOAbbreviation>Neurology</ISOAbbreviation></Journal><ArticleTitle>Mechanisms compensating for dopamine loss in early Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>S32-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1212/WNL.0b013e318198e0e9</ELocationID><Abstract><AbstractText>Parkinson disease (PD) is a disorder with a substantive period before the emergence of motor symptoms, during which significant dopaminergic neuronal loss is counterbalanced by endogenous compensatory mechanisms. Many potential compensatory mechanisms have now been proposed; these are both dopaminergic, focused on enhancing effects or exposure to existing dopamine, and nondopaminergic, being focused on reducing activity of the indirect striatal output pathway. Compensatory mechanisms can potentially postpone and reduce the severity of parkinsonian symptoms, and contribute to the benefit provided by a symptomatic therapy, thus offering targets for novel therapeutics. However, enhancement of certain compensatory mechanisms may produce problems when subsequent therapies are initiated, e.g., the development of motor complications with levodopa. Supporting endogenous compensatory mechanisms, to delay or reverse apparent disease progression, is a novel and attractive "disease-modifying" approach to PD. Such actions may contribute to the apparent disease-modifying benefit of initiating early treatment with levodopa or rasagiline, as suggested by the ELLDOPA and TEMPO studies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Brotchie</LastName><ForeName>Jonathan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Toronto Western Research Institute, University Health Network, Toronto, Canada. brotchie@uhnres.utoronto.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fitzer-Attas</LastName><ForeName>Cheryl</ForeName><Initials>C</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurology</MedlineTA><NlmUniqueID>0401060</NlmUniqueID><ISSNLinking>0028-3878</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007189">Indans</NameOfSubstance></Chemical><Chemical><RegistryNumber>003N66TS6T</RegistryNumber><NameOfSubstance UI="C031967">rasagiline</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005917" MajorTopicYN="N">Globus Pallidus</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007189" MajorTopicYN="N">Indans</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009434" MajorTopicYN="N">Neural Pathways</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>78</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>2</Month><Day>18</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>3</Month><Day>3</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>3</Month><Day>13</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19221312</ArticleId><ArticleId IdType="pii">72/7_Supplement_2/S32</ArticleId><ArticleId IdType="doi">10.1212/WNL.0b013e318198e0e9</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Fitzer Attas, Cheryl" sort="Fitzer Attas, Cheryl" uniqKey="Fitzer Attas C" first="Cheryl" last="Fitzer-Attas">Cheryl Fitzer-Attas</name></noCountry><country name="Canada"><noRegion><name sortKey="Brotchie, Jonathan" sort="Brotchie, Jonathan" uniqKey="Brotchie J" first="Jonathan" last="Brotchie">Jonathan Brotchie</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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