Brain iron and ferritin in Parkinson's and Alzheimer's diseases
Identifieur interne : 000701 ( Main/Corpus ); précédent : 000700; suivant : 000702Brain iron and ferritin in Parkinson's and Alzheimer's diseases
Auteurs : K. Jellinger ; W. Paulus ; I. Grundke-Iqbal ; P. Riederer ; H. YoudimSource :
- Journal of Neural Transmission - Parkinson's Disease and Dementia Section [ 0936-3076 ] ; 1990-12-01.
Abstract
Summary: Semiquantitative histological evaluation of brain iron and ferritin in Parkinson's (PD) and Alzheimer's disease (DAT) have been performed in paraffin sections of brain regions which included frontal cortex, hippocampus, basal ganglia and brain stem. The results indicate a significant selective increase of Fe3+ and ferritin in substantia nigra zona compacta but not in zona reticulata of Parkinsonian brains, confirming the biochemical estimation of iron. No such changes were observed in the same regions of DAT brains. The increase of iron is evident in astrocytes, macrophages, reactive microglia and non-pigmented neurons, and in damaged areas devoid of pigmented neurons. In substantia nigra of PD and PD/DAT, strong ferritin reactivity was also associated with proliferated microglia. A faint iron staining was seen occasionally in peripheral halo of Lewy bodies. By contrast, in DAT and PD/DAT, strong ferritin immunoreactivity was observed in and around senile plaques and neurofibrillary tangles. The interrelationship between selective increase of iron and ferritin in PD requires further investigation, because both changes could participate in the induction of oxidative stress and neuronal dath, due to their ability to promote formation of oxygen radicals.
Url:
DOI: 10.1007/BF02252926
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ISTEX:31DEF3A95E218CB4FBA4985E3AFEA21CF500FFE6Le document en format XML
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Grundke-Iqbal</name><affiliation><mods:affiliation>NYS Institute for Basic Research in Developmental Disabilities, Staten Island, N. Y., USA</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 School of Medicine, Würzburg, Federal Republic of Germany</mods:affiliation></affiliation></author><author><name sortKey="Youdim, H" sort="Youdim, H" uniqKey="Youdim H" first="H." last="Youdim">H. Youdim</name><affiliation><mods:affiliation>Department of Pharmacology, Technion, Faculty of Medicine, Haifa, Israel</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:31DEF3A95E218CB4FBA4985E3AFEA21CF500FFE6</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1007/BF02252926</idno><idno type="url">https://api.istex.fr/document/31DEF3A95E218CB4FBA4985E3AFEA21CF500FFE6/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000701</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Brain iron and ferritin in Parkinson's and Alzheimer's diseases</title><author><name sortKey="Jellinger, K" sort="Jellinger, K" uniqKey="Jellinger K" first="K." last="Jellinger">K. Jellinger</name><affiliation><mods:affiliation>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</mods:affiliation></affiliation></author><author><name sortKey="Paulus, W" sort="Paulus, W" uniqKey="Paulus W" first="W." last="Paulus">W. Paulus</name><affiliation><mods:affiliation>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</mods:affiliation></affiliation></author><author><name sortKey="Grundke Iqbal, I" sort="Grundke Iqbal, I" uniqKey="Grundke Iqbal I" first="I." last="Grundke-Iqbal">I. Grundke-Iqbal</name><affiliation><mods:affiliation>NYS Institute for Basic Research in Developmental Disabilities, Staten Island, N. Y., USA</mods:affiliation></affiliation></author><author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. 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Youdim</name><affiliation><mods:affiliation>Department of Pharmacology, Technion, Faculty of Medicine, Haifa, Israel</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title><title level="j" type="abbrev">J Neural Transm Gen Sect</title><idno type="ISSN">0936-3076</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1990-12-01">1990-12-01</date><biblScope unit="volume">2</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="327">327</biblScope><biblScope unit="page" to="340">340</biblScope></imprint><idno type="ISSN">0936-3076</idno></series><idno type="istex">31DEF3A95E218CB4FBA4985E3AFEA21CF500FFE6</idno><idno type="DOI">10.1007/BF02252926</idno><idno type="ArticleID">Art8</idno><idno type="ArticleID">BF02252926</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0936-3076</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Semiquantitative histological evaluation of brain iron and ferritin in Parkinson's (PD) and Alzheimer's disease (DAT) have been performed in paraffin sections of brain regions which included frontal cortex, hippocampus, basal ganglia and brain stem. The results indicate a significant selective increase of Fe3+ and ferritin in substantia nigra zona compacta but not in zona reticulata of Parkinsonian brains, confirming the biochemical estimation of iron. No such changes were observed in the same regions of DAT brains. The increase of iron is evident in astrocytes, macrophages, reactive microglia and non-pigmented neurons, and in damaged areas devoid of pigmented neurons. In substantia nigra of PD and PD/DAT, strong ferritin reactivity was also associated with proliferated microglia. A faint iron staining was seen occasionally in peripheral halo of Lewy bodies. By contrast, in DAT and PD/DAT, strong ferritin immunoreactivity was observed in and around senile plaques and neurofibrillary tangles. The interrelationship between selective increase of iron and ferritin in PD requires further investigation, because both changes could participate in the induction of oxidative stress and neuronal dath, due to their ability to promote formation of oxygen radicals.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>Prof. Dr. K. Jellinger</name><affiliations><json:string>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</json:string></affiliations></json:item><json:item><name>W. Paulus</name><affiliations><json:string>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</json:string></affiliations></json:item><json:item><name>I. Grundke-Iqbal</name><affiliations><json:string>NYS Institute for Basic Research in Developmental Disabilities, Staten Island, N. Y., USA</json:string></affiliations></json:item><json:item><name>P. Riederer</name><affiliations><json:string>Clinical Neurochemistry, Department of Psychiatry, University of Würzburg School of Medicine, Würzburg, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>M. B. H. Youdim</name><affiliations><json:string>Department of Pharmacology, Technion, Faculty of Medicine, Haifa, Israel</json:string></affiliations></json:item></author><articleId><json:string>Art8</json:string><json:string>BF02252926</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: Semiquantitative histological evaluation of brain iron and ferritin in Parkinson's (PD) and Alzheimer's disease (DAT) have been performed in paraffin sections of brain regions which included frontal cortex, hippocampus, basal ganglia and brain stem. The results indicate a significant selective increase of Fe3+ and ferritin in substantia nigra zona compacta but not in zona reticulata of Parkinsonian brains, confirming the biochemical estimation of iron. No such changes were observed in the same regions of DAT brains. The increase of iron is evident in astrocytes, macrophages, reactive microglia and non-pigmented neurons, and in damaged areas devoid of pigmented neurons. In substantia nigra of PD and PD/DAT, strong ferritin reactivity was also associated with proliferated microglia. A faint iron staining was seen occasionally in peripheral halo of Lewy bodies. By contrast, in DAT and PD/DAT, strong ferritin immunoreactivity was observed in and around senile plaques and neurofibrillary tangles. 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G. Joshi, Department of Biochemistry, University of Tennessee, Knoxville, TN, U.S.A.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Brain iron and ferritin in Parkinson's and Alzheimer's diseases</title><author><persName><forename type="first">K.</forename><surname>Jellinger</surname></persName><roleName type="degree">Prof. Dr.</roleName><affiliation>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</affiliation></author><author><persName><forename type="first">W.</forename><surname>Paulus</surname></persName><affiliation>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</affiliation></author><author><persName><forename type="first">I.</forename><surname>Grundke-Iqbal</surname></persName><affiliation>NYS Institute for Basic Research in Developmental Disabilities, Staten Island, N. 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The results indicate a significant selective increase of Fe3+ and ferritin in substantia nigra zona compacta but not in zona reticulata of Parkinsonian brains, confirming the biochemical estimation of iron. No such changes were observed in the same regions of DAT brains. The increase of iron is evident in astrocytes, macrophages, reactive microglia and non-pigmented neurons, and in damaged areas devoid of pigmented neurons. In substantia nigra of PD and PD/DAT, strong ferritin reactivity was also associated with proliferated microglia. A faint iron staining was seen occasionally in peripheral halo of Lewy bodies. By contrast, in DAT and PD/DAT, strong ferritin immunoreactivity was observed in and around senile plaques and neurofibrillary tangles. The interrelationship between selective increase of iron and ferritin in PD requires further investigation, because both changes could participate in the induction of oxidative stress and neuronal dath, due to their ability to promote formation of oxygen radicals.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Psychiatry</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1990-08-02">Created</change><change when="1990-12-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">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/31DEF3A95E218CB4FBA4985E3AFEA21CF500FFE6/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>722</JournalID><JournalPrintISSN>0936-3076</JournalPrintISSN><JournalElectronicISSN>1435-1463</JournalElectronicISSN><JournalTitle>Journal of Neural Transmission - Parkinson's Disease and Dementia Section</JournalTitle><JournalAbbreviatedTitle>J Neural Transm Gen Sect</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Pharmacology/Toxicology</JournalSubject><JournalSubject Type="Secondary">Psychiatry</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd><IssueArticleCount>9</IssueArticleCount><IssueHistory><CoverDate><DateString>1990</DateString><Year>1990</Year><Month>12</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1990</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art8"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF02252926</ArticleID><ArticleDOI>10.1007/BF02252926</ArticleDOI><ArticleSequenceNumber>8</ArticleSequenceNumber><ArticleTitle Language="En">Brain iron and ferritin in Parkinson's and Alzheimer's diseases</ArticleTitle><ArticleCategory>Full Papers</ArticleCategory><ArticleFirstPage>327</ArticleFirstPage><ArticleLastPage>340</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>10</Month><Day>25</Day></RegistrationDate><Received><Year>1990</Year><Month>8</Month><Day>2</Day></Received><Accepted><Year>1990</Year><Month>10</Month><Day>4</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1990</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>722</JournalID><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><IssueIDStart>4</IssueIDStart><IssueIDEnd>4</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><Prefix>Prof. Dr.</Prefix><GivenName>K.</GivenName><FamilyName>Jellinger</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>W.</GivenName><FamilyName>Paulus</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>I.</GivenName><FamilyName>Grundke-Iqbal</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><FamilyName>Riederer</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>Ludwig Boltzmann Institute of Clinical Neurobiology</OrgDivision><OrgName>Lainz Hospital</OrgName><OrgAddress><Street>Wolkersbergenstrasse 1</Street><Postcode>A-1130</Postcode><City>Vienna</City><Country>Austria</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>NYS Institute for Basic Research in Developmental Disabilities</OrgName><OrgAddress><City>Staten Island</City><State>N. Y.</State><Country>USA</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Clinical Neurochemistry, Department of Psychiatry</OrgDivision><OrgName>University of Würzburg School of Medicine</OrgName><OrgAddress><City>Würzburg</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation><Affiliation ID="Aff4"><OrgDivision>Department of Pharmacology</OrgDivision><OrgName>Technion, Faculty of Medicine</OrgName><OrgAddress><City>Haifa</City><Country>Israel</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Semiquantitative histological evaluation of brain iron and ferritin in Parkinson's (PD) and Alzheimer's disease (DAT) have been performed in paraffin sections of brain regions which included frontal cortex, hippocampus, basal ganglia and brain stem. The results indicate a significant selective increase of Fe<Superscript>3+</Superscript> and ferritin in substantia nigra zona compacta but not in zona reticulata of Parkinsonian brains, confirming the biochemical estimation of iron. No such changes were observed in the same regions of DAT brains. The increase of iron is evident in astrocytes, macrophages, reactive microglia and non-pigmented neurons, and in damaged areas devoid of pigmented neurons. In substantia nigra of PD and PD/DAT, strong ferritin reactivity was also associated with proliferated microglia. A faint iron staining was seen occasionally in peripheral halo of Lewy bodies. By contrast, in DAT and PD/DAT, strong ferritin immunoreactivity was observed in and around senile plaques and neurofibrillary tangles. The interrelationship between selective increase of iron and ferritin in PD requires further investigation, because both changes could participate in the induction of oxidative stress and neuronal dath, due to their ability to promote formation of oxygen radicals.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Iron</Keyword><Keyword>ferritin</Keyword><Keyword>Parkinson's disease</Keyword><Keyword>Alzheimer's disease</Keyword><Keyword>melanin</Keyword><Keyword>Lewy body</Keyword></KeywordGroup><ArticleNote Type="Misc"><SimplePara>Ferritin antisera were kindly provided by Dr. J. G. Joshi, Department of Biochemistry, University of Tennessee, Knoxville, TN, U.S.A.</SimplePara></ArticleNote></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Brain iron and ferritin in Parkinson's and Alzheimer's diseases</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Brain iron and ferritin in Parkinson's and Alzheimer's diseases</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Prof. Dr.</namePart><namePart type="given">K.</namePart><namePart type="family">Jellinger</namePart><affiliation>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="family">Paulus</namePart><affiliation>Ludwig Boltzmann Institute of Clinical Neurobiology, Lainz Hospital, Wolkersbergenstrasse 1, A-1130, Vienna, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">I.</namePart><namePart type="family">Grundke-Iqbal</namePart><affiliation>NYS Institute for Basic Research in Developmental Disabilities, Staten Island, N. Y., USA</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 School of Medicine, Würzburg, Federal Republic of Germany</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, Technion, Faculty of Medicine, 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">1990-08-02</dateCreated><dateIssued encoding="w3cdtf">1990-12-01</dateIssued><copyrightDate encoding="w3cdtf">1990</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: Semiquantitative histological evaluation of brain iron and ferritin in Parkinson's (PD) and Alzheimer's disease (DAT) have been performed in paraffin sections of brain regions which included frontal cortex, hippocampus, basal ganglia and brain stem. The results indicate a significant selective increase of Fe3+ and ferritin in substantia nigra zona compacta but not in zona reticulata of Parkinsonian brains, confirming the biochemical estimation of iron. No such changes were observed in the same regions of DAT brains. The increase of iron is evident in astrocytes, macrophages, reactive microglia and non-pigmented neurons, and in damaged areas devoid of pigmented neurons. In substantia nigra of PD and PD/DAT, strong ferritin reactivity was also associated with proliferated microglia. A faint iron staining was seen occasionally in peripheral halo of Lewy bodies. By contrast, in DAT and PD/DAT, strong ferritin immunoreactivity was observed in and around senile plaques and neurofibrillary tangles. The interrelationship between selective increase of iron and ferritin in PD requires further investigation, because both changes could participate in the induction of oxidative stress and neuronal dath, due to their ability to promote formation of oxygen radicals.</abstract><note>Full Papers</note><note>Ferritin antisera were kindly provided by Dr. J. G. 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