Brain stem pathology in Parkinson's disease: An evaluation of the Braak staging model
Identifieur interne : 000898 ( Istex/Corpus ); précédent : 000897; suivant : 000899Brain stem pathology in Parkinson's disease: An evaluation of the Braak staging model
Auteurs : Ann E. Kingsbury ; Rina Bandopadhyay ; Laura Silveira-Moriyama ; Hilary Ayling ; Constantinos Kallis ; William Sterlacci ; Hans Maeir ; Werner Poewe ; Andrew J. LeesSource :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
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Abstract
The lower brain stem of 25 pathologically‐confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy‐type α‐synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically‐normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo‐rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23305
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Kingsbury</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Bandopadhyay, Rina" sort="Bandopadhyay, Rina" uniqKey="Bandopadhyay R" first="Rina" last="Bandopadhyay">Rina Bandopadhyay</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Silveira Oriyama, Laura" sort="Silveira Oriyama, Laura" uniqKey="Silveira Oriyama L" first="Laura" last="Silveira-Moriyama">Laura Silveira-Moriyama</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Ayling, Hilary" sort="Ayling, Hilary" uniqKey="Ayling H" first="Hilary" last="Ayling">Hilary Ayling</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Kallis, Constantinos" sort="Kallis, Constantinos" uniqKey="Kallis C" first="Constantinos" last="Kallis">Constantinos Kallis</name><affiliation><mods:affiliation>Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Sterlacci, William" sort="Sterlacci, William" uniqKey="Sterlacci W" first="William" last="Sterlacci">William Sterlacci</name><affiliation><mods:affiliation>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Maeir, Hans" sort="Maeir, Hans" uniqKey="Maeir H" first="Hans" last="Maeir">Hans Maeir</name><affiliation><mods:affiliation>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><mods:affiliation>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</mods:affiliation></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew J. 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All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically‐normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo‐rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ann E. Kingsbury PhD</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Rina Bandopadhyay PhD</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Laura Silveira‐Moriyama MD, PhD</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Hilary Ayling MSc</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Constantinos Kallis PhD</name><affiliations><json:string>Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom</json:string></affiliations></json:item><json:item><name>William Sterlacci MD</name><affiliations><json:string>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Hans Maeir MD</name><affiliations><json:string>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Werner Poewe MD</name><affiliations><json:string>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</json:string></affiliations></json:item><json:item><name>Andrew J. Lees F. Med. Sci.</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</json:string><json:string>Queen Square Brain Bank for Neurological Disorders, UCL, Institute of Neurology, London, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Lewy body pathology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pathology staging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>medulla oblongata</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dorsal motor nucleus of the vagus</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The lower brain stem of 25 pathologically‐confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy‐type α‐synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically‐normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. 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Med. Sci.</roleName></persName><affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation><affiliation>Queen Square Brain Bank for Neurological Disorders, UCL, Institute of Neurology, London, United Kingdom</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-11-15"></date><biblScope unit="vol">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2508">2508</biblScope><biblScope unit="page" to="2515">2515</biblScope></imprint></monogr><idno type="istex">6623685F8973DCA0DE9E322B3B0D4CBF1AFC2990</idno><idno type="DOI">10.1002/mds.23305</idno><idno type="ArticleID">MDS23305</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The lower brain stem of 25 pathologically‐confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy‐type α‐synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically‐normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo‐rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Lewy body pathology</term></item><item><term>pathology staging</term></item><item><term>medulla oblongata</term></item><item><term>dorsal motor nucleus of the vagus</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-02-11">Received</change><change when="2010-05-17">Registration</change><change when="2010-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6623685F8973DCA0DE9E322B3B0D4CBF1AFC2990/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="150"><doi origin="wiley" registered="yes">10.1002/mds.v25:15</doi><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">15</numbering></numberingGroup><coverDate startDate="2010-11-15">15 November 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="50" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23305</doi><idGroup><id type="unit" value="MDS23305"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-02-11"></event><event type="manuscriptRevised" date="2010-03-28"></event><event type="manuscriptAccepted" date="2010-05-17"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.1.9 mode:FullText" date="2013-01-24"></event><event type="publishedOnlineEarlyUnpaginated" date="2010-09-03"></event><event type="publishedOnlineFinalForm" date="2010-11-10"></event><event type="firstOnline" date="2010-09-03"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">2508</numbering><numbering type="pageLast">2515</numbering></numberingGroup><correspondenceTo>Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23305.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="31"></count><count type="wordTotal" number="5061"></count></countGroup><titleGroup><title type="main" xml:lang="en">Brain stem pathology in Parkinson's disease: An evaluation of the Braak staging model</title><title type="short" xml:lang="en">Brain Stem Pathology in Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Ann E.</givenNames><familyName>Kingsbury</familyName><degrees>PhD</degrees></personName><contactDetails><email>a.kingsbury@ion.ucl.ac.uk</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Rina</givenNames><familyName>Bandopadhyay</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Laura</givenNames><familyName>Silveira‐Moriyama</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Hilary</givenNames><familyName>Ayling</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Constantinos</givenNames><familyName>Kallis</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3"><personName><givenNames>William</givenNames><familyName>Sterlacci</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Hans</givenNames><familyName>Maeir</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Werner</givenNames><familyName>Poewe</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1 #af4"><personName><givenNames>Andrew J.</givenNames><familyName>Lees</familyName><degrees>F. Med. Sci.</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="AT" type="organization"><unparsedAffiliation>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="GB" type="organization"><unparsedAffiliation>Queen Square Brain Bank for Neurological Disorders, UCL, Institute of Neurology, London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">Lewy body pathology</keyword><keyword xml:id="kwd3">pathology staging</keyword><keyword xml:id="kwd4">medulla oblongata</keyword><keyword xml:id="kwd5">dorsal motor nucleus of the vagus</keyword></keywordGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23305:MDS_23305_sm_suppinfo"></mediaResource><caption>Supporting Information</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The lower brain stem of 25 pathologically‐confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy‐type α‐synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically‐normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo‐rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1" numbered="no"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Brain stem pathology in Parkinson's disease: An evaluation of the Braak staging model</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Brain Stem Pathology in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Brain stem pathology in Parkinson's disease: An evaluation of the Braak staging model</title></titleInfo><name type="personal"><namePart type="given">Ann E.</namePart><namePart type="family">Kingsbury</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation><description>Correspondence: Institute of Neurology, 1 Wakefield Street, London WC1N 1PJ, UK</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rina</namePart><namePart type="family">Bandopadhyay</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Laura</namePart><namePart type="family">Silveira‐Moriyama</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hilary</namePart><namePart type="family">Ayling</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Constantinos</namePart><namePart type="family">Kallis</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Medical Statistics Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">William</namePart><namePart type="family">Sterlacci</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hans</namePart><namePart type="family">Maeir</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Werner</namePart><namePart type="family">Poewe</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew J.</namePart><namePart type="family">Lees</namePart><namePart type="termsOfAddress">F. Med. Sci.</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom</affiliation><affiliation>Queen Square Brain Bank for Neurological Disorders, UCL, Institute of Neurology, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-11-15</dateIssued><dateCaptured encoding="w3cdtf">2010-02-11</dateCaptured><dateValid encoding="w3cdtf">2010-05-17</dateValid><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">1</extent><extent unit="references">31</extent><extent unit="words">5061</extent></physicalDescription><abstract lang="en">The lower brain stem of 25 pathologically‐confirmed Parkinson's disease (PD) cases was examined by alpha synuclein immunohistochemistry to characterize pathological accumulation of alpha synuclein (Lewy‐type α‐synucleinopathy, LTS) in the medulla oblongata, to examine differences between affected regions and test a proposed model of staging of pathology in PD. All cases had LTS in the medulla, including the dorsal motor nucleus of the vagus (dmX), when present. The distribution followed a consistent pattern and appeared to be concentrated in a tyrosine hydroxylase (TH) immunoreactive region, probably representing the dorsal IX/X nuclear complex and the intermediate reticular zone. LTS density was greatest in the dmX. A similar distribution pattern to PD was seen in 14 incidental Lewy body disease (ILBD) cases, five derived from the Queen Square Brain Bank tissue collection and nine identified in separate series of 60 neurologically‐normal individuals, and in three cases with the G2019S mutation of LRRK2. Semiquantitative assessment showed that severity of pathology in the dmX was not correlated with the severity of cortical pathology. Semiquantitative assay of TH and ChAT peptide expression in the medulla showed that TH expression in PD and ILBD did not differ from controls. These findings broadly support the Braak hypothesis of caudo‐rostral development but indicate that the extent of the disease in the cortex and the severity of pathology in the medulla were independent of one another. © 2010 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Lewy body pathology</topic><topic>pathology staging</topic><topic>medulla oblongata</topic><topic>dorsal motor nucleus of the vagus</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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