Brain stem pathology in Parkinson's disease: an evaluation of the Braak staging model.
Identifieur interne : 002E45 ( Ncbi/Merge ); précédent : 002E44; suivant : 002E46Brain stem pathology in Parkinson's disease: an evaluation of the Braak staging model.
Auteurs : Ann E. Kingsbury [Royaume-Uni] ; Rina Bandopadhyay ; Laura Silveira-Moriyama ; Hilary Ayling ; Constantinos Kallis ; William Sterlacci ; Hans Maeir ; Werner Poewe [Autriche] ; Andrew J. LeesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Aged, Brain Stem (metabolism), Brain Stem (pathology), Female, Humans, Immunohistochemistry, Lewy Bodies (metabolism), Lewy Bodies (pathology), Lewy Body Disease (pathology), Male, Middle Aged, Neurons (metabolism), Neurons (pathology), Odds Ratio, Parkinson Disease (metabolism), Parkinson Disease (pathology), Severity of Illness Index, Tyrosine 3-Monooxygenase (metabolism), alpha-Synuclein (metabolism).
- MESH :
- chemical , metabolism : Tyrosine 3-Monooxygenase, alpha-Synuclein.
- metabolism : Brain Stem, Lewy Bodies, Neurons, Parkinson Disease.
- pathology : Brain Stem, Lewy Bodies, Lewy Body Disease, Neurons, Parkinson Disease.
- Aged, Female, Humans, Immunohistochemistry, Male, Middle Aged, Odds Ratio, Severity of Illness Index.
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.
DOI: 10.1002/mds.23305
PubMed: 20818670
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Kingsbury</name><affiliation wicri:level="3"><nlm:affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom. a.kingsbury@ion.ucl.ac.uk</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Bandopadhyay, Rina" sort="Bandopadhyay, Rina" uniqKey="Bandopadhyay R" first="Rina" last="Bandopadhyay">Rina Bandopadhyay</name></author><author><name sortKey="Silveira Moriyama, Laura" sort="Silveira Moriyama, Laura" uniqKey="Silveira Moriyama L" first="Laura" last="Silveira-Moriyama">Laura Silveira-Moriyama</name></author><author><name sortKey="Ayling, Hilary" sort="Ayling, Hilary" uniqKey="Ayling H" first="Hilary" last="Ayling">Hilary Ayling</name></author><author><name sortKey="Kallis, Constantinos" sort="Kallis, Constantinos" uniqKey="Kallis C" first="Constantinos" last="Kallis">Constantinos Kallis</name></author><author><name sortKey="Sterlacci, William" sort="Sterlacci, William" uniqKey="Sterlacci W" first="William" last="Sterlacci">William Sterlacci</name></author><author><name sortKey="Maeir, Hans" sort="Maeir, Hans" uniqKey="Maeir H" first="Hans" last="Maeir">Hans Maeir</name></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></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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Kingsbury</name><affiliation wicri:level="3"><nlm:affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom. a.kingsbury@ion.ucl.ac.uk</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Bandopadhyay, Rina" sort="Bandopadhyay, Rina" uniqKey="Bandopadhyay R" first="Rina" last="Bandopadhyay">Rina Bandopadhyay</name></author><author><name sortKey="Silveira Moriyama, Laura" sort="Silveira Moriyama, Laura" uniqKey="Silveira Moriyama L" first="Laura" last="Silveira-Moriyama">Laura Silveira-Moriyama</name></author><author><name sortKey="Ayling, Hilary" sort="Ayling, Hilary" uniqKey="Ayling H" first="Hilary" last="Ayling">Hilary Ayling</name></author><author><name sortKey="Kallis, Constantinos" sort="Kallis, Constantinos" uniqKey="Kallis C" first="Constantinos" last="Kallis">Constantinos Kallis</name></author><author><name sortKey="Sterlacci, William" sort="Sterlacci, William" uniqKey="Sterlacci W" first="William" last="Sterlacci">William Sterlacci</name></author><author><name sortKey="Maeir, Hans" sort="Maeir, Hans" uniqKey="Maeir H" first="Hans" last="Maeir">Hans Maeir</name></author><author><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name><affiliation><country>Autriche</country><placeName><settlement type="city">Innsbruck</settlement><region nuts="2" type="region">Tyrol (Land)</region></placeName><orgName type="university">Université de médecine d'Innsbruck</orgName></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J" last="Lees">Andrew J. Lees</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Brain Stem (metabolism)</term><term>Brain Stem (pathology)</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Lewy Bodies (metabolism)</term><term>Lewy Bodies (pathology)</term><term>Lewy Body Disease (pathology)</term><term>Male</term><term>Middle Aged</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Odds Ratio</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Severity of Illness Index</term><term>Tyrosine 3-Monooxygenase (metabolism)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tyrosine 3-Monooxygenase</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain Stem</term><term>Lewy Bodies</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain Stem</term><term>Lewy Bodies</term><term>Lewy Body Disease</term><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Male</term><term>Middle Aged</term><term>Odds Ratio</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20818670</PMID><DateCreated><Year>2010</Year><Month>11</Month><Day>11</Day></DateCreated><DateCompleted><Year>2011</Year><Month>02</Month><Day>25</Day></DateCompleted><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>15</Issue><PubDate><Year>2010</Year><Month>Nov</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Brain stem pathology in Parkinson's disease: an evaluation of the Braak staging model.</ArticleTitle><Pagination><MedlinePgn>2508-15</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23305</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>© 2010 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kingsbury</LastName><ForeName>Ann E</ForeName><Initials>AE</Initials><AffiliationInfo><Affiliation>Reta Lila Weston Institute of Neurological Studies, UCL, Institute of Neurology, London, United Kingdom. a.kingsbury@ion.ucl.ac.uk</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bandopadhyay</LastName><ForeName>Rina</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Silveira-Moriyama</LastName><ForeName>Laura</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Ayling</LastName><ForeName>Hilary</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Kallis</LastName><ForeName>Constantinos</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Sterlacci</LastName><ForeName>William</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Maeir</LastName><ForeName>Hans</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Poewe</LastName><ForeName>Werner</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Lees</LastName><ForeName>Andrew J</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.16.2</RegistryNumber><NameOfSubstance UI="D014446">Tyrosine 3-Monooxygenase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001933">Brain Stem</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007150">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016631">Lewy Bodies</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D020961">Lewy Body Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016017">Odds Ratio</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012720">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014446">Tyrosine 3-Monooxygenase</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D051844">alpha-Synuclein</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>9</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>2</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.23305</ArticleId><ArticleId IdType="pubmed">20818670</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Autriche</li><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li><li>Tyrol (Land)</li></region><settlement><li>Innsbruck</li><li>Londres</li></settlement><orgName><li>Université de médecine d'Innsbruck</li></orgName></list><tree><noCountry><name sortKey="Ayling, Hilary" sort="Ayling, Hilary" uniqKey="Ayling H" first="Hilary" last="Ayling">Hilary Ayling</name><name sortKey="Bandopadhyay, Rina" sort="Bandopadhyay, Rina" uniqKey="Bandopadhyay R" first="Rina" last="Bandopadhyay">Rina Bandopadhyay</name><name sortKey="Kallis, Constantinos" sort="Kallis, Constantinos" uniqKey="Kallis C" first="Constantinos" last="Kallis">Constantinos Kallis</name><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J" last="Lees">Andrew J. Lees</name><name sortKey="Maeir, Hans" sort="Maeir, Hans" uniqKey="Maeir H" first="Hans" last="Maeir">Hans Maeir</name><name sortKey="Silveira Moriyama, Laura" sort="Silveira Moriyama, Laura" uniqKey="Silveira Moriyama L" first="Laura" last="Silveira-Moriyama">Laura Silveira-Moriyama</name><name sortKey="Sterlacci, William" sort="Sterlacci, William" uniqKey="Sterlacci W" first="William" last="Sterlacci">William Sterlacci</name></noCountry><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Kingsbury, Ann E" sort="Kingsbury, Ann E" uniqKey="Kingsbury A" first="Ann E" last="Kingsbury">Ann E. Kingsbury</name></region></country><country name="Autriche"><region name="Tyrol (Land)"><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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