α‐Synuclein pathology of the spinal and peripheral autonomic nervous system in neurologically unimpaired elderly subjects
Identifieur interne : 000915 ( Main/Corpus ); précédent : 000914; suivant : 000916α‐Synuclein pathology of the spinal and peripheral autonomic nervous system in neurologically unimpaired elderly subjects
Auteurs : A. Bloch ; A. Probst ; H. Bissig ; H. Adams ; M. TolnaySource :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 2006-06.
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Abstract
Studies on cases with incidental Lewy body disease (ILBD) suggest that α‐synuclein (αSN) pathology of Parkinson's disease (PD) starts in lower brainstem nuclei and in the olfactory bulb. However, medullary structures as the induction site of αSN pathology have been questioned as large parts of the nervous system, including the spinal cord and the peripheral autonomic nervous system (PANS), have not been examined in ILBD. Thus, the time course of PD lesions in the spinal cord or PANS in relation to medullary lesions remains unknown. We collected 98 post mortem cases with no reference to PD‐associated symptoms on clinical records. αSN pathology was found in the central nervous system, including the spinal cord, and in the PANS in 17 (17.3%) cases. αSN pathology was encountered in autonomic nuclei of the thoracic spinal cord, brainstem and olfactory nerves in 17/17, in sacral parasympathetic nuclei in 15/16, in the myenteric plexus of oesophagus in 14/17, in sympathetic ganglia in 14/17, and in the vagus nerve in 12/16 cases. In addition to the thoracic lateral horns, a high number of αSN lesions was also found in non‐autonomic spinal cord nuclei. Considering supraspinal structures our cases corresponded roughly to the recently described sequential order of αSN involvement in PD. Our study indicates, however, that the autonomic nuclei of the spinal cord and the PANS belong to the most constantly and earliest affected regions next to medullary structures and the olfactory nerves. A larger cohort of ILBD cases will be needed to pinpoint the precise induction site of αSN pathology among these structures.
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DOI: 10.1111/j.1365-2990.2006.00727.x
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However, medullary structures as the induction site of αSN pathology have been questioned as large parts of the nervous system, including the spinal cord and the peripheral autonomic nervous system (PANS), have not been examined in ILBD. Thus, the time course of PD lesions in the spinal cord or PANS in relation to medullary lesions remains unknown. We collected 98 post mortem cases with no reference to PD‐associated symptoms on clinical records. αSN pathology was found in the central nervous system, including the spinal cord, and in the PANS in 17 (17.3%) cases. αSN pathology was encountered in autonomic nuclei of the thoracic spinal cord, brainstem and olfactory nerves in 17/17, in sacral parasympathetic nuclei in 15/16, in the myenteric plexus of oesophagus in 14/17, in sympathetic ganglia in 14/17, and in the vagus nerve in 12/16 cases. In addition to the thoracic lateral horns, a high number of αSN lesions was also found in non‐autonomic spinal cord nuclei. Considering supraspinal structures our cases corresponded roughly to the recently described sequential order of αSN involvement in PD. Our study indicates, however, that the autonomic nuclei of the spinal cord and the PANS belong to the most constantly and earliest affected regions next to medullary structures and the olfactory nerves. A larger cohort of ILBD cases will be needed to pinpoint the precise induction site of αSN pathology among these structures.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>A. Bloch</name><affiliations><json:string>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</json:string></affiliations></json:item><json:item><name>A. Probst</name><affiliations><json:string>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</json:string></affiliations></json:item><json:item><name>H. 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However, medullary structures as the induction site of αSN pathology have been questioned as large parts of the nervous system, including the spinal cord and the peripheral autonomic nervous system (PANS), have not been examined in ILBD. Thus, the time course of PD lesions in the spinal cord or PANS in relation to medullary lesions remains unknown. We collected 98 post mortem cases with no reference to PD‐associated symptoms on clinical records. αSN pathology was found in the central nervous system, including the spinal cord, and in the PANS in 17 (17.3%) cases. αSN pathology was encountered in autonomic nuclei of the thoracic spinal cord, brainstem and olfactory nerves in 17/17, in sacral parasympathetic nuclei in 15/16, in the myenteric plexus of oesophagus in 14/17, in sympathetic ganglia in 14/17, and in the vagus nerve in 12/16 cases. In addition to the thoracic lateral horns, a high number of αSN lesions was also found in non‐autonomic spinal cord nuclei. Considering supraspinal structures our cases corresponded roughly to the recently described sequential order of αSN involvement in PD. Our study indicates, however, that the autonomic nuclei of the spinal cord and the PANS belong to the most constantly and earliest affected regions next to medullary structures and the olfactory nerves. A larger cohort of ILBD cases will be needed to pinpoint the precise induction site of αSN pathology among these structures.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>α‐synuclein</term></item><item><term>autonomic nervous system</term></item><item><term>incidental Lewy body disease</term></item><item><term>Lewy bodies</term></item><item><term>Lewy neurites</term></item><item><term>Parkinson's disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/723ADF43379CF2E95E18D5B6A936512CAF5E10F6/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2990</doi><issn type="print">0305-1846</issn><issn type="electronic">1365-2990</issn><idGroup><id type="product" value="NAN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="NEUROPATHOLOGY APPLIED NEUROBIOLOGY">Neuropathology and Applied Neurobiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="06003"><doi origin="wiley">10.1111/nan.2006.32.issue-3</doi><numberingGroup><numbering type="journalVolume" number="32">32</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2006-06">June 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="5" status="forIssue"><doi origin="wiley">10.1111/j.1365-2990.2006.00727.x</doi><idGroup><id type="unit" value="NAN727"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">Original articles</title></titleGroup><eventGroup><event type="firstOnline" date="2006-04-25"></event><event type="publishedOnlineFinalForm" date="2006-04-25"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.15 mode:FullText source:FullText result:FullText" date="2010-07-19"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-03"></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" number="284">284</numbering><numbering type="pageLast" number="295">295</numbering></numberingGroup><correspondenceTo>Markus Tolnay, Institute of Pathology, Department of Neuropathology, Schoenbeinstrasse 40, CH‐4031 Basel, Switzerland. Tel: +41 61 265 2525; Fax: +41 61 265 3194; E‐mail: <email>mtolnay@uhbs.ch</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NAN.NAN727.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received September 29, 2005 Accepted after revision January 10, 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="6"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="5468"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">α‐Synuclein pathology of the spinal and peripheral autonomic nervous system in neurologically unimpaired elderly subjects</title><title type="shortAuthors">A. Bloch <i>et al.</i></title><title type="short">α‐Synuclein pathology of the autonomic nervous system</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>A.</givenNames><familyName>Bloch</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#aff-1-1"><personName><givenNames>A.</givenNames><familyName>Probst</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#aff-1-1"><personName><givenNames>H.</givenNames><familyName>Bissig</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#aff-1-1"><personName><givenNames>H.</givenNames><familyName>Adams</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#aff-1-1"><personName><givenNames>M.</givenNames><familyName>Tolnay</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="CH"><unparsedAffiliation>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">α‐synuclein</keyword><keyword xml:id="k2">autonomic nervous system</keyword><keyword xml:id="k3">incidental Lewy body disease</keyword><keyword xml:id="k4">Lewy bodies</keyword><keyword xml:id="k5">Lewy neurites</keyword><keyword xml:id="k6">Parkinson's disease </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!-- A. Bloch, A. Probst, H. Bissig, H. Adams and M. Tolnay (2006) Neuropathology and Applied Neurobiology 32, 284–295
α-Synuclein pathology of the spinal and peripheral autonomic nervous system in neurologically unimpaired elderly subjects --><p>Studies on cases with incidental Lewy body disease (ILBD) suggest that α‐synuclein (αSN) pathology of Parkinson's disease (PD) starts in lower brainstem nuclei and in the olfactory bulb. However, medullary structures as the induction site of αSN pathology have been questioned as large parts of the nervous system, including the spinal cord and the peripheral autonomic nervous system (PANS), have not been examined in ILBD. Thus, the time course of PD lesions in the spinal cord or PANS in relation to medullary lesions remains unknown. We collected 98 <i>post mortem</i> cases with no reference to PD‐associated symptoms on clinical records. αSN pathology was found in the central nervous system, including the spinal cord, and in the PANS in 17 (17.3%) cases. αSN pathology was encountered in autonomic nuclei of the thoracic spinal cord, brainstem and olfactory nerves in 17/17, in sacral parasympathetic nuclei in 15/16, in the myenteric plexus of oesophagus in 14/17, in sympathetic ganglia in 14/17, and in the vagus nerve in 12/16 cases. In addition to the thoracic lateral horns, a high number of αSN lesions was also found in non‐autonomic spinal cord nuclei. Considering supraspinal structures our cases corresponded roughly to the recently described sequential order of αSN involvement in PD. Our study indicates, however, that the autonomic nuclei of the spinal cord and the PANS belong to the most constantly and earliest affected regions next to medullary structures and the olfactory nerves. A larger cohort of ILBD cases will be needed to pinpoint the precise induction site of αSN pathology among these structures.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>α‐Synuclein pathology of the spinal and peripheral autonomic nervous system in neurologically unimpaired elderly subjects</title></titleInfo><titleInfo type="abbreviated"><title>α‐Synuclein pathology of the autonomic nervous system</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>α‐Synuclein pathology of the spinal and peripheral autonomic nervous system in neurologically unimpaired elderly subjects</title></titleInfo><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Bloch</namePart><affiliation>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Probst</namePart><affiliation>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Bissig</namePart><affiliation>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Adams</namePart><affiliation>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Tolnay</namePart><affiliation>Institute of Pathology, Department of Neuropathology, University Hospital Basel, Basel, Switzerland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-06</dateIssued><edition>Received September 29, 2005 Accepted after revision January 10, 2005</edition><copyrightDate encoding="w3cdtf">2006</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">1</extent><extent unit="tables">6</extent><extent unit="references">33</extent><extent unit="words">5468</extent></physicalDescription><abstract lang="en">Studies on cases with incidental Lewy body disease (ILBD) suggest that α‐synuclein (αSN) pathology of Parkinson's disease (PD) starts in lower brainstem nuclei and in the olfactory bulb. However, medullary structures as the induction site of αSN pathology have been questioned as large parts of the nervous system, including the spinal cord and the peripheral autonomic nervous system (PANS), have not been examined in ILBD. Thus, the time course of PD lesions in the spinal cord or PANS in relation to medullary lesions remains unknown. We collected 98 post mortem cases with no reference to PD‐associated symptoms on clinical records. αSN pathology was found in the central nervous system, including the spinal cord, and in the PANS in 17 (17.3%) cases. αSN pathology was encountered in autonomic nuclei of the thoracic spinal cord, brainstem and olfactory nerves in 17/17, in sacral parasympathetic nuclei in 15/16, in the myenteric plexus of oesophagus in 14/17, in sympathetic ganglia in 14/17, and in the vagus nerve in 12/16 cases. In addition to the thoracic lateral horns, a high number of αSN lesions was also found in non‐autonomic spinal cord nuclei. Considering supraspinal structures our cases corresponded roughly to the recently described sequential order of αSN involvement in PD. Our study indicates, however, that the autonomic nuclei of the spinal cord and the PANS belong to the most constantly and earliest affected regions next to medullary structures and the olfactory nerves. A larger cohort of ILBD cases will be needed to pinpoint the precise induction site of αSN pathology among these structures.</abstract><subject lang="en"><genre>Keywords</genre><topic>α‐synuclein</topic><topic>autonomic nervous system</topic><topic>incidental Lewy body disease</topic><topic>Lewy bodies</topic><topic>Lewy neurites</topic><topic>Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>Neuropathology and Applied Neurobiology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0305-1846</identifier><identifier type="eISSN">1365-2990</identifier><identifier type="DOI">10.1111/(ISSN)1365-2990</identifier><identifier type="PublisherID">NAN</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>32</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>284</start><end>295</end><total>12</total></extent></part></relatedItem><identifier type="istex">723ADF43379CF2E95E18D5B6A936512CAF5E10F6</identifier><identifier type="DOI">10.1111/j.1365-2990.2006.00727.x</identifier><identifier type="ArticleID">NAN727</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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