Neuropathological features of multiple system atrophy with cognitive impairment.
Identifieur interne : 000539 ( PubMed/Curation ); précédent : 000538; suivant : 000540Neuropathological features of multiple system atrophy with cognitive impairment.
Auteurs : Y T Asi [Royaume-Uni] ; Helen Ling ; Z. Ahmed ; A J Lees ; T. Revesz ; J L HoltonSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2014.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Brain (pathology), Cognition (physiology), Cognition Disorders (etiology), Cognition Disorders (pathology), Female, Humans, Male, Middle Aged, Multiple System Atrophy (complications), Multiple System Atrophy (pathology), Nerve Degeneration (complications), Nerve Degeneration (pathology), Neurons (pathology).
- MESH :
- complications : Multiple System Atrophy, Nerve Degeneration.
- etiology : Cognition Disorders.
- pathology : Brain, Cognition Disorders, Multiple System Atrophy, Nerve Degeneration, Neurons.
- physiology : Cognition.
- Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged.
Abstract
Cognitive impairment (CI) is an exclusion criterion for the diagnosis of multiple system atrophy (MSA), according to the second consensus statement. This view was recently challenged by patients with pathologically confirmed MSA who were reported to have dementia. With an aim to investigate the pathological substrate of CI in MSA, quantitative assessment of the glial and neuronal cytoplasmic inclusions and semiquantitative assessment of neuronal loss in the cortical and limbic regions was performed. No differences in the severity of these MSA-related pathological findings were identified between nine MSA cases with CI and nine MSA cases with normal cognition. Alzheimer's-related pathological changes, cerebral amyloid angiopathy, and cerebrovascular disease did not differ between the two MSA groups. MSA-specific α-synuclein and secondary pathological conditions were not more severe in MSA cases with CI, suggesting that although CI may be intrinsic to the MSA disease process, further investigation into the pathological basis of cognitive impairment in MSA is warranted.
DOI: 10.1002/mds.25887
PubMed: 24752994
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Ahmed</name></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name></author><author><name sortKey="Revesz, T" sort="Revesz, T" uniqKey="Revesz T" first="T" last="Revesz">T. 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Ahmed</name></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A J" last="Lees">A J Lees</name></author><author><name sortKey="Revesz, T" sort="Revesz, T" uniqKey="Revesz T" first="T" last="Revesz">T. Revesz</name></author><author><name sortKey="Holton, J L" sort="Holton, J L" uniqKey="Holton J" first="J L" last="Holton">J L Holton</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="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Brain (pathology)</term><term>Cognition (physiology)</term><term>Cognition Disorders (etiology)</term><term>Cognition Disorders (pathology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Multiple System Atrophy (complications)</term><term>Multiple System Atrophy (pathology)</term><term>Nerve Degeneration (complications)</term><term>Nerve Degeneration (pathology)</term><term>Neurons (pathology)</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Multiple System Atrophy</term><term>Nerve Degeneration</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Cognition Disorders</term><term>Multiple System Atrophy</term><term>Nerve Degeneration</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Cognition</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cognitive impairment (CI) is an exclusion criterion for the diagnosis of multiple system atrophy (MSA), according to the second consensus statement. This view was recently challenged by patients with pathologically confirmed MSA who were reported to have dementia. With an aim to investigate the pathological substrate of CI in MSA, quantitative assessment of the glial and neuronal cytoplasmic inclusions and semiquantitative assessment of neuronal loss in the cortical and limbic regions was performed. No differences in the severity of these MSA-related pathological findings were identified between nine MSA cases with CI and nine MSA cases with normal cognition. Alzheimer's-related pathological changes, cerebral amyloid angiopathy, and cerebrovascular disease did not differ between the two MSA groups. MSA-specific α-synuclein and secondary pathological conditions were not more severe in MSA cases with CI, suggesting that although CI may be intrinsic to the MSA disease process, further investigation into the pathological basis of cognitive impairment in MSA is warranted.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">24752994</PMID><DateCreated><Year>2014</Year><Month>06</Month><Day>13</Day></DateCreated><DateCompleted><Year>2015</Year><Month>02</Month><Day>26</Day></DateCompleted><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>7</Issue><PubDate><Year>2014</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Neuropathological features of multiple system atrophy with cognitive impairment.</ArticleTitle><Pagination><MedlinePgn>884-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25887</ELocationID><Abstract><AbstractText>Cognitive impairment (CI) is an exclusion criterion for the diagnosis of multiple system atrophy (MSA), according to the second consensus statement. This view was recently challenged by patients with pathologically confirmed MSA who were reported to have dementia. With an aim to investigate the pathological substrate of CI in MSA, quantitative assessment of the glial and neuronal cytoplasmic inclusions and semiquantitative assessment of neuronal loss in the cortical and limbic regions was performed. No differences in the severity of these MSA-related pathological findings were identified between nine MSA cases with CI and nine MSA cases with normal cognition. Alzheimer's-related pathological changes, cerebral amyloid angiopathy, and cerebrovascular disease did not differ between the two MSA groups. MSA-specific α-synuclein and secondary pathological conditions were not more severe in MSA cases with CI, suggesting that although CI may be intrinsic to the MSA disease process, further investigation into the pathological basis of cognitive impairment in MSA is warranted.</AbstractText><CopyrightInformation>© 2014 International Parkinson and Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Asi</LastName><ForeName>Y T</ForeName><Initials>YT</Initials><AffiliationInfo><Affiliation>Queen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ling</LastName><ForeName>Helen</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Ahmed</LastName><ForeName>Z</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Lees</LastName><ForeName>A J</ForeName><Initials>AJ</Initials></Author><Author ValidYN="Y"><LastName>Revesz</LastName><ForeName>T</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Holton</LastName><ForeName>J L</ForeName><Initials>JL</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>04</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000369">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003071">Cognition</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003072">Cognition Disorders</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</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="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019578">Multiple System Atrophy</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009410">Nerve Degeneration</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009474">Neurons</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">MSA</Keyword><Keyword MajorTopicYN="N">cognitive impairment</Keyword><Keyword MajorTopicYN="N">dementia</Keyword><Keyword MajorTopicYN="N">neuropathology</Keyword><Keyword MajorTopicYN="N">α-synuclein</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>10</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>3</Month><Day>8</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>3</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="aheadofprint"><Year>2014</Year><Month>4</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>4</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>4</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>2</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24752994</ArticleId><ArticleId 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