Increased iron (III) and total iron content in post mortem substantia nigra of parkinsonian brain
Identifieur interne : 002855 ( Main/Corpus ); précédent : 002854; suivant : 002856Increased iron (III) and total iron content in post mortem substantia nigra of parkinsonian brain
Auteurs : E. Sofic ; P. Riederer ; H. Heinsen ; H. Beckmann ; P. Reynolds ; G. Hebenstreit ; H. YoudimSource :
- Journal of Neural Transmission [ 0300-9564 ] ; 1988-10-01.
Abstract
Summary: Significant differences in the content of iron (III) and total iron were found in post mortem substantia nigra of Parkinson's disease. There was an increase of 176% in the levels of total iron and 255% of iron (III) in the substantia nigra of the parkinsonian patients compared to age matched controls. In the cortex (Brodmann area 21), hippocampus, putamen, and globus pallidus there was no significant difference in the levels of iron (III) and total iron. Thus the changes in total iron, iron (III) and the iron (II)/iron (III) ratio in the parkinsonian substantia nigra are likely to be involved in the pathophysiology and treatment of this disorder.
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DOI: 10.1007/BF01244786
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Increased iron (III) and total iron content in post mortem substantia nigra of parkinsonian brain</title><author><name sortKey="Sofic, E" sort="Sofic, E" uniqKey="Sofic E" first="E." last="Sofic">E. Sofic</name><affiliation><mods:affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name><affiliation><mods:affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Heinsen, H" sort="Heinsen, H" uniqKey="Heinsen H" first="H." last="Heinsen">H. Heinsen</name><affiliation><mods:affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Beckmann, H" sort="Beckmann, H" uniqKey="Beckmann H" first="H." last="Beckmann">H. Beckmann</name><affiliation><mods:affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Reynolds, P" sort="Reynolds, P" uniqKey="Reynolds P" first="P." last="Reynolds">P. Reynolds</name><affiliation><mods:affiliation>Department of Pathology, University of Nottingham, Nottingham, UK</mods:affiliation></affiliation></author><author><name sortKey="Hebenstreit, G" sort="Hebenstreit, G" uniqKey="Hebenstreit G" first="G." last="Hebenstreit">G. 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Sofic</name><affiliation><mods:affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name><affiliation><mods:affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Heinsen, H" sort="Heinsen, H" uniqKey="Heinsen H" first="H." last="Heinsen">H. Heinsen</name><affiliation><mods:affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Beckmann, H" sort="Beckmann, H" uniqKey="Beckmann H" first="H." last="Beckmann">H. 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Neural Transmission</title><idno type="ISSN">0300-9564</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1988-10-01">1988-10-01</date><biblScope unit="volume">74</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="199">199</biblScope><biblScope unit="page" to="205">205</biblScope></imprint><idno type="ISSN">0300-9564</idno></series><idno type="istex">FC024056FDC37B5C8B7AAC717C79D040D5FDA637</idno><idno type="DOI">10.1007/BF01244786</idno><idno type="ArticleID">Art8</idno><idno type="ArticleID">BF01244786</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0300-9564</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Significant differences in the content of iron (III) and total iron were found in post mortem substantia nigra of Parkinson's disease. There was an increase of 176% in the levels of total iron and 255% of iron (III) in the substantia nigra of the parkinsonian patients compared to age matched controls. In the cortex (Brodmann area 21), hippocampus, putamen, and globus pallidus there was no significant difference in the levels of iron (III) and total iron. Thus the changes in total iron, iron (III) and the iron (II)/iron (III) ratio in the parkinsonian substantia nigra are likely to be involved in the pathophysiology and treatment of this disorder.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>E. Sofic</name><affiliations><json:string>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>P. 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In the cortex (Brodmann area 21), hippocampus, putamen, and globus pallidus there was no significant difference in the levels of iron (III) and total iron. 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Neural Transmission</title><idno type="JournalID">702</idno><idno type="pISSN">0300-9564</idno><idno type="eISSN">1435-1463</idno><idno type="IssueArticleCount">10</idno><idno type="VolumeIssueCount">3</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1988-10-01"></date><biblScope unit="volume">74</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="199">199</biblScope><biblScope unit="page" to="205">205</biblScope></imprint></monogr><idno type="istex">FC024056FDC37B5C8B7AAC717C79D040D5FDA637</idno><idno type="DOI">10.1007/BF01244786</idno><idno type="ArticleID">Art8</idno><idno type="ArticleID">BF01244786</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1988-06-08</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Summary: Significant differences in the content of iron (III) and total iron were found in post mortem substantia nigra of Parkinson's disease. There was an increase of 176% in the levels of total iron and 255% of iron (III) in the substantia nigra of the parkinsonian patients compared to age matched controls. In the cortex (Brodmann area 21), hippocampus, putamen, and globus pallidus there was no significant difference in the levels of iron (III) and total iron. Thus the changes in total iron, iron (III) and the iron (II)/iron (III) ratio in the parkinsonian substantia nigra are likely to be involved in the pathophysiology and treatment of this disorder.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Neurology</term></item><item><term>Psychiatry</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1988-06-08">Created</change><change when="1988-10-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-1">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/FC024056FDC37B5C8B7AAC717C79D040D5FDA637/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Vienna</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>702</JournalID><JournalPrintISSN>0300-9564</JournalPrintISSN><JournalElectronicISSN>1435-1463</JournalElectronicISSN><JournalTitle>Journal of Neural Transmission</JournalTitle><JournalSubTitle>Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</JournalSubTitle><JournalAbbreviatedTitle>J. Neural Transmission</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Pharmacology/Toxicology</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject><JournalSubject Type="Secondary">Psychiatry</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>74</VolumeIDStart><VolumeIDEnd>74</VolumeIDEnd><VolumeIssueCount>3</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>3</IssueIDStart><IssueIDEnd>3</IssueIDEnd><IssueArticleCount>10</IssueArticleCount><IssueHistory><CoverDate><DateString>1988</DateString><Year>1988</Year><Month>10</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1988</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art8"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF01244786</ArticleID><ArticleDOI>10.1007/BF01244786</ArticleDOI><ArticleSequenceNumber>8</ArticleSequenceNumber><ArticleTitle Language="En">Increased iron (III) and total iron content in post mortem substantia nigra of parkinsonian brain</ArticleTitle><ArticleCategory>Short Note</ArticleCategory><ArticleFirstPage>199</ArticleFirstPage><ArticleLastPage>205</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>2</Month><Day>16</Day></RegistrationDate><Received><Year>1988</Year><Month>6</Month><Day>8</Day></Received><Accepted><Year>1988</Year><Month>8</Month><Day>31</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer Verlag</CopyrightHolderName><CopyrightYear>1988</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>702</JournalID><VolumeIDStart>74</VolumeIDStart><VolumeIDEnd>74</VolumeIDEnd><IssueIDStart>3</IssueIDStart><IssueIDEnd>3</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>E.</GivenName><FamilyName>Sofic</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><FamilyName>Riederer</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>H.</GivenName><FamilyName>Heinsen</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>H.</GivenName><FamilyName>Beckmann</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>G.</GivenName><GivenName>P.</GivenName><FamilyName>Reynolds</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>G.</GivenName><FamilyName>Hebenstreit</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff4"><AuthorName DisplayOrder="Western"><GivenName>M.</GivenName><GivenName>B.</GivenName><GivenName>H.</GivenName><FamilyName>Youdim</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgDivision>Clinical Neurochemistry, Department of Psychiatry</OrgDivision><OrgName>University of Würzburg</OrgName><OrgAddress><City>Würzburg</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgDivision>Department of Pathology</OrgDivision><OrgName>University of Nottingham</OrgName><OrgAddress><City>Nottingham</City><Country>UK</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgName>Niederösterreichisches Landeskrankenhaus für Psychiatrie und Neurologie</OrgName><OrgAddress><City>Mauer-Öhlig</City><State>Mauer</State><Country>Austria</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Department of Pharmacology</OrgDivision><OrgName>Rappaport Family Research Institute, Faculty of Medicine</OrgName><OrgAddress><City>Technion, Haifa</City><Country>Israel</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Significant differences in the content of iron (III) and total iron were found in post mortem substantia nigra of Parkinson's disease. There was an increase of 176% in the levels of total iron and 255% of iron (III) in the substantia nigra of the parkinsonian patients compared to age matched controls. In the cortex (<Emphasis Type="Italic">Brodmann area 21</Emphasis>), hippocampus, putamen, and globus pallidus there was no significant difference in the levels of iron (III) and total iron. Thus the changes in total iron, iron (III) and the iron (II)/iron (III) ratio in the parkinsonian substantia nigra are likely to be involved in the pathophysiology and treatment of this disorder.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Total iron</Keyword><Keyword>iron (III)</Keyword><Keyword>iron (II)</Keyword><Keyword>iron (II)/iron (III) ratio</Keyword><Keyword>Parkinson's disease</Keyword><Keyword>neurotoxicity</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Increased iron (III) and total iron content in post mortem substantia nigra of parkinsonian brain</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Increased iron (III) and total iron content in post mortem substantia nigra of parkinsonian brain</title></titleInfo><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Sofic</namePart><affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Riederer</namePart><affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Heinsen</namePart><affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Beckmann</namePart><affiliation>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg, Würzburg, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="given">P.</namePart><namePart type="family">Reynolds</namePart><affiliation>Department of Pathology, University of Nottingham, Nottingham, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Hebenstreit</namePart><affiliation>Niederösterreichisches Landeskrankenhaus für Psychiatrie und Neurologie, Mauer-Öhlig, Mauer, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="given">B.</namePart><namePart type="given">H.</namePart><namePart type="family">Youdim</namePart><affiliation>Department of Pharmacology, Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1988-06-08</dateCreated><dateIssued encoding="w3cdtf">1988-10-01</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Significant differences in the content of iron (III) and total iron were found in post mortem substantia nigra of Parkinson's disease. There was an increase of 176% in the levels of total iron and 255% of iron (III) in the substantia nigra of the parkinsonian patients compared to age matched controls. In the cortex (Brodmann area 21), hippocampus, putamen, and globus pallidus there was no significant difference in the levels of iron (III) and total iron. Thus the changes in total iron, iron (III) and the iron (II)/iron (III) ratio in the parkinsonian substantia nigra are likely to be involved in the pathophysiology and treatment of this disorder.</abstract><note>Short Note</note><relatedItem type="host"><titleInfo><title>Journal of Neural Transmission</title><subTitle>Basic neurosciences and genetics, Parkinson's disease and allied conditions, Alzheimer's disease and related disorders, biological psychiatry</subTitle></titleInfo><titleInfo type="abbreviated"><title>J. Neural Transmission</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1988-10-01</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pharmacology/Toxicology</topic><topic>Neurology</topic><topic>Psychiatry</topic></subject><identifier type="ISSN">0300-9564</identifier><identifier type="eISSN">1435-1463</identifier><identifier type="JournalID">702</identifier><identifier type="IssueArticleCount">10</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>1988</date><detail type="volume"><number>74</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="pages"><start>199</start><end>205</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1988</recordOrigin></recordInfo></relatedItem><identifier type="istex">FC024056FDC37B5C8B7AAC717C79D040D5FDA637</identifier><identifier type="DOI">10.1007/BF01244786</identifier><identifier type="ArticleID">Art8</identifier><identifier type="ArticleID">BF01244786</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer Verlag, 1988</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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