The protective role of levodopa in the human substantia nigra.
Identifieur interne : 001587 ( PubMed/Curation ); précédent : 001586; suivant : 001588The protective role of levodopa in the human substantia nigra.
Auteurs : A H Rajput [Canada]Source :
- Advances in neurology [ 0091-3952 ] ; 2001.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Antiparkinson Agents, Levodopa, Neuroprotective Agents.
- drug effects : Substantia Nigra.
- drug therapy : Parkinson Disease.
- physiopathology : Substantia Nigra.
- Adult, Animals, Child, Female, Humans, Male, Middle Aged.
Abstract
Laboratory studies and studies of animal models of parkinsonism have produced contradictory evidence, but there is no evidence that LD is toxic to normal substantia nigra in animals. We have studied human subjects longitudinally to address that issue. A cumulative LD dose up to 24 kg was not toxic in one autopsied essential tremor (ET) case. Two other ET patients did not develop parkinsonism on 8.5 kg and 21 kg cumulative LD dose, respectively. One DOPA-responsive dystonia (DRD) case has no evidence of parkinsonism after 29 years and more than 17 kg of LD. A DRD patient who received 3 kg over 11 years had normal SN neuronal complement at autopsy. One patient who has clinical and laboratory evidence of nigral pathology as the basis of parkinsonism when untreated for 18 years had progressive disability. While on LD he has excellent symptomatic benefit and virtual cessation of progression of the disease. Epidemiologic studies indicate that those prescribed LD at an early stage of illness and hence given larger cumulative lifetime doses have longer survival than those in whom LD is started late and who receive smaller total doses. Our observations and the available literature support that levodopa is not toxic to normal or diseased substantia nigra in human beings. Evidence presented here indicates that levodopa has a protective effect on the human substantia nigra neurons.
PubMed: 11553992
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We have studied human subjects longitudinally to address that issue. A cumulative LD dose up to 24 kg was not toxic in one autopsied essential tremor (ET) case. Two other ET patients did not develop parkinsonism on 8.5 kg and 21 kg cumulative LD dose, respectively. One DOPA-responsive dystonia (DRD) case has no evidence of parkinsonism after 29 years and more than 17 kg of LD. A DRD patient who received 3 kg over 11 years had normal SN neuronal complement at autopsy. One patient who has clinical and laboratory evidence of nigral pathology as the basis of parkinsonism when untreated for 18 years had progressive disability. While on LD he has excellent symptomatic benefit and virtual cessation of progression of the disease. Epidemiologic studies indicate that those prescribed LD at an early stage of illness and hence given larger cumulative lifetime doses have longer survival than those in whom LD is started late and who receive smaller total doses. Our observations and the available literature support that levodopa is not toxic to normal or diseased substantia nigra in human beings. Evidence presented here indicates that levodopa has a protective effect on the human substantia nigra neurons.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11553992</PMID><DateCreated><Year>2001</Year><Month>09</Month><Day>13</Day></DateCreated><DateCompleted><Year>2002</Year><Month>02</Month><Day>04</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0091-3952</ISSN><JournalIssue CitedMedium="Print"><Volume>86</Volume><PubDate><Year>2001</Year></PubDate></JournalIssue><Title>Advances in neurology</Title><ISOAbbreviation>Adv Neurol</ISOAbbreviation></Journal><ArticleTitle>The protective role of levodopa in the human substantia nigra.</ArticleTitle><Pagination><MedlinePgn>327-36</MedlinePgn></Pagination><Abstract><AbstractText>Laboratory studies and studies of animal models of parkinsonism have produced contradictory evidence, but there is no evidence that LD is toxic to normal substantia nigra in animals. We have studied human subjects longitudinally to address that issue. A cumulative LD dose up to 24 kg was not toxic in one autopsied essential tremor (ET) case. Two other ET patients did not develop parkinsonism on 8.5 kg and 21 kg cumulative LD dose, respectively. One DOPA-responsive dystonia (DRD) case has no evidence of parkinsonism after 29 years and more than 17 kg of LD. A DRD patient who received 3 kg over 11 years had normal SN neuronal complement at autopsy. One patient who has clinical and laboratory evidence of nigral pathology as the basis of parkinsonism when untreated for 18 years had progressive disability. While on LD he has excellent symptomatic benefit and virtual cessation of progression of the disease. Epidemiologic studies indicate that those prescribed LD at an early stage of illness and hence given larger cumulative lifetime doses have longer survival than those in whom LD is started late and who receive smaller total doses. Our observations and the available literature support that levodopa is not toxic to normal or diseased substantia nigra in human beings. Evidence presented here indicates that levodopa has a protective effect on the human substantia nigra neurons.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rajput</LastName><ForeName>A H</ForeName><Initials>AH</Initials><AffiliationInfo><Affiliation>Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, S7N 0W8, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Adv Neurol</MedlineTA><NlmUniqueID>0367524</NlmUniqueID><ISSNLinking>0091-3952</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" 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="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>71</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2001</Year><Month>9</Month><Day>14</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>2</Month><Day>5</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2001</Year><Month>9</Month><Day>14</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11553992</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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