Is the vulnerability of neurons in the substantia nigra of patients with Parkinson's disease related to their neuromelanin content?
Identifieur interne : 001754 ( PubMed/Corpus ); précédent : 001753; suivant : 001755Is the vulnerability of neurons in the substantia nigra of patients with Parkinson's disease related to their neuromelanin content?
Auteurs : A. Kastner ; E C Hirsch ; O. Lejeune ; F. Javoy-Agid ; O. Rascol ; Y. AgidSource :
- Journal of neurochemistry [ 0022-3042 ] ; 1992.
English descriptors
- KwdEn :
- Aged, Densitometry, Female, Humans, Image Processing, Computer-Assisted, Male, Melanins (metabolism), Mesencephalon (cytology), Mesencephalon (metabolism), Middle Aged, Neurons (metabolism), Neurons (physiology), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Reference Values, Substantia Nigra (metabolism), Substantia Nigra (pathology), Substantia Nigra (physiopathology), Tissue Distribution.
- MESH :
- chemical , metabolism : Melanins.
- cytology : Mesencephalon.
- metabolism : Mesencephalon, Neurons, Parkinson Disease, Substantia Nigra.
- pathology : Parkinson Disease, Substantia Nigra.
- physiology : Neurons.
- physiopathology : Parkinson Disease, Substantia Nigra.
- Aged, Densitometry, Female, Humans, Image Processing, Computer-Assisted, Male, Middle Aged, Reference Values, Tissue Distribution.
Abstract
The contribution of neuromelanin (NM) to the pathogenesis of Parkinson's disease (PD) has long been suspected. In particular, a correlation has been reported between the estimated cell loss in the mesencephalic dopaminergic cell groups and the percentage of NM-pigmented neurons in these cell groups. To test whether the amount of pigment per cell is a critical factor or whether the presence of NM within a neuron is sufficient to account for the degeneration of dopaminergic neurons, the NM content was measured in each neuron from representative sections throughout the ventral mesencephalon of four controls subjects and four patients with PD. Intraneuronal NM was quantified by a densitometric method, using known amounts of synthetic melanin as standards. In control brains, the distribution of melanized neurons in the nigral complex showed a high proportion of lightly melanized neurons in the ventral tegmental area and the pars alpha and gamma of the substantia nigra (SN), whereas heavily melanized neurons were mostly located in the pars beta and lateralis of the SN. An inverse relationship was observed between the percentage of surviving neurons in PD compared with controls and the amount of NM they contain, suggesting that the vulnerability of the dopaminergic neurons is related to their NM content. Factors other than NM may be involved in the differential vulnerability of catecholaminergic neurons in PD. In particular, the constant topography of the cell loss suggests that cell position within the nigral complex is a key factor.
PubMed: 1494900
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Rascol</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1992">1992</date><idno type="RBID">pubmed:1494900</idno><idno type="pmid">1494900</idno><idno type="wicri:Area/PubMed/Corpus">001754</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001754</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Is the vulnerability of neurons in the substantia nigra of patients with Parkinson's disease related to their neuromelanin content?</title><author><name sortKey="Kastner, A" sort="Kastner, A" uniqKey="Kastner A" first="A" last="Kastner">A. Kastner</name><affiliation><nlm:affiliation>INSERM U. 289, Hôpital de la Salpêtrière, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name></author><author><name sortKey="Lejeune, O" sort="Lejeune, O" uniqKey="Lejeune O" first="O" last="Lejeune">O. Lejeune</name></author><author><name sortKey="Javoy Agid, F" sort="Javoy Agid, F" uniqKey="Javoy Agid F" first="F" last="Javoy-Agid">F. Javoy-Agid</name></author><author><name sortKey="Rascol, O" sort="Rascol, O" uniqKey="Rascol O" first="O" last="Rascol">O. Rascol</name></author><author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Y. Agid</name></author></analytic><series><title level="j">Journal of neurochemistry</title><idno type="ISSN">0022-3042</idno><imprint><date when="1992" type="published">1992</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Densitometry</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Male</term><term>Melanins (metabolism)</term><term>Mesencephalon (cytology)</term><term>Mesencephalon (metabolism)</term><term>Middle Aged</term><term>Neurons (metabolism)</term><term>Neurons (physiology)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Reference Values</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>Substantia Nigra (physiopathology)</term><term>Tissue Distribution</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Melanins</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Mesencephalon</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mesencephalon</term><term>Neurons</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Densitometry</term><term>Female</term><term>Humans</term><term>Image Processing, Computer-Assisted</term><term>Male</term><term>Middle Aged</term><term>Reference Values</term><term>Tissue Distribution</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The contribution of neuromelanin (NM) to the pathogenesis of Parkinson's disease (PD) has long been suspected. In particular, a correlation has been reported between the estimated cell loss in the mesencephalic dopaminergic cell groups and the percentage of NM-pigmented neurons in these cell groups. To test whether the amount of pigment per cell is a critical factor or whether the presence of NM within a neuron is sufficient to account for the degeneration of dopaminergic neurons, the NM content was measured in each neuron from representative sections throughout the ventral mesencephalon of four controls subjects and four patients with PD. Intraneuronal NM was quantified by a densitometric method, using known amounts of synthetic melanin as standards. In control brains, the distribution of melanized neurons in the nigral complex showed a high proportion of lightly melanized neurons in the ventral tegmental area and the pars alpha and gamma of the substantia nigra (SN), whereas heavily melanized neurons were mostly located in the pars beta and lateralis of the SN. An inverse relationship was observed between the percentage of surviving neurons in PD compared with controls and the amount of NM they contain, suggesting that the vulnerability of the dopaminergic neurons is related to their NM content. Factors other than NM may be involved in the differential vulnerability of catecholaminergic neurons in PD. In particular, the constant topography of the cell loss suggests that cell position within the nigral complex is a key factor.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1494900</PMID><DateCreated><Year>1992</Year><Month>09</Month><Day>09</Day></DateCreated><DateCompleted><Year>1992</Year><Month>09</Month><Day>09</Day></DateCompleted><DateRevised><Year>2004</Year><Month>11</Month><Day>17</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3042</ISSN><JournalIssue CitedMedium="Print"><Volume>59</Volume><Issue>3</Issue><PubDate><Year>1992</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Is the vulnerability of neurons in the substantia nigra of patients with Parkinson's disease related to their neuromelanin content?</ArticleTitle><Pagination><MedlinePgn>1080-9</MedlinePgn></Pagination><Abstract><AbstractText>The contribution of neuromelanin (NM) to the pathogenesis of Parkinson's disease (PD) has long been suspected. In particular, a correlation has been reported between the estimated cell loss in the mesencephalic dopaminergic cell groups and the percentage of NM-pigmented neurons in these cell groups. To test whether the amount of pigment per cell is a critical factor or whether the presence of NM within a neuron is sufficient to account for the degeneration of dopaminergic neurons, the NM content was measured in each neuron from representative sections throughout the ventral mesencephalon of four controls subjects and four patients with PD. Intraneuronal NM was quantified by a densitometric method, using known amounts of synthetic melanin as standards. In control brains, the distribution of melanized neurons in the nigral complex showed a high proportion of lightly melanized neurons in the ventral tegmental area and the pars alpha and gamma of the substantia nigra (SN), whereas heavily melanized neurons were mostly located in the pars beta and lateralis of the SN. An inverse relationship was observed between the percentage of surviving neurons in PD compared with controls and the amount of NM they contain, suggesting that the vulnerability of the dopaminergic neurons is related to their NM content. Factors other than NM may be involved in the differential vulnerability of catecholaminergic neurons in PD. In particular, the constant topography of the cell loss suggests that cell position within the nigral complex is a key factor.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kastner</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>INSERM U. 289, Hôpital de la Salpêtrière, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirsch</LastName><ForeName>E C</ForeName><Initials>EC</Initials></Author><Author ValidYN="Y"><LastName>Lejeune</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Javoy-Agid</LastName><ForeName>F</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Rascol</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Agid</LastName><ForeName>Y</ForeName><Initials>Y</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008543">Melanins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C014121">neuromelanin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>J Neurochem. 1993 May;60(5):1976-7</RefSource><PMID Version="1">8473913</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003720" MajorTopicYN="N">Densitometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007091" MajorTopicYN="N">Image Processing, Computer-Assisted</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008543" MajorTopicYN="N">Melanins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008636" MajorTopicYN="N">Mesencephalon</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012016" MajorTopicYN="N">Reference Values</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013378" MajorTopicYN="N">Substantia Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014018" MajorTopicYN="N">Tissue Distribution</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1992</Year><Month>9</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1992</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1992</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">1494900</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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