MovDisordV3, PubMed, Checkpoint, bibRecord, 003E54

The pathogenesis of multiple system atrophy: past, present, and future.

Identifieur interne : 003E54 ( PubMed/Checkpoint ); précédent : 003E53; suivant : 003E55

The pathogenesis of multiple system atrophy: past, present, and future.

Auteurs : E. Jaros [Royaume-Uni] ; D J Burn

Source :

Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2000.

RBID : pubmed:11009180

English descriptors

KwdEn :
- Biological Markers, Brain (metabolism), Brain (pathology), Gene Expression Regulation, Genes, Regulator, Humans, Inclusion Bodies (metabolism), Inclusion Bodies (pathology), Multiple System Atrophy (classification), Multiple System Atrophy (etiology), Multiple System Atrophy (genetics), Multiple System Atrophy (metabolism), Multiple System Atrophy (pathology), Mutation, Nerve Tissue Proteins (genetics), Nerve Tissue Proteins (metabolism), Neuregulins (genetics), Oligodendroglia (metabolism), Oligodendroglia (pathology), Polymorphism, Genetic, Synucleins, alpha-Synuclein, tau Proteins (metabolism).
MESH :
- chemical , genetics : Nerve Tissue Proteins, Neuregulins.
- chemical , metabolism : Nerve Tissue Proteins, tau Proteins.
- chemical : Biological Markers, Synucleins, alpha-Synuclein.
- classification : Multiple System Atrophy.
- etiology : Multiple System Atrophy.
- genetics : Multiple System Atrophy.
- metabolism : Brain, Inclusion Bodies, Multiple System Atrophy, Oligodendroglia.
- pathology : Brain, Inclusion Bodies, Multiple System Atrophy, Oligodendroglia.
- Gene Expression Regulation, Genes, Regulator, Humans, Mutation, Polymorphism, Genetic.

Abstract

Multiple system atrophy is a sporadic, adult-onset neurodegenerative disease of unknown etiology. The condition may be unique among neurodegenerative diseases by the prominent, if not primary, role played by the oligodendroglial cell in the pathogenetic process. Recent developments in our understanding of multiple system atrophy have included the detection of glial cytoplasmic inclusions and alpha-synuclein accumulation in these inclusions. The latter finding links multiple system atrophy as an "alpha-synucleinopathy" to Parkinson's disease and dementia with Lewy bodies. This article reviews recent important findings of potential relevance to the pathogenesis of multiple system atrophy. We also speculate on areas in which further advances may be made to progress our understanding of this devastating condition.

PubMed: 11009180

Affiliations:

Royaume-Uni

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: 003F25
to stream PubMed, to step Curation: 003F25

Links to Exploration step

pubmed:11009180

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The pathogenesis of multiple system atrophy: past, present, and future.</title>
<author><name sortKey="Jaros, E" sort="Jaros, E" uniqKey="Jaros E" first="E" last="Jaros">E. Jaros</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Neuropathology, Newcastle General Hospital, Newcastle upon Tyne, UK.</nlm:affiliation>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Department of Neuropathology, Newcastle General Hospital, Newcastle upon Tyne</wicri:regionArea>
<wicri:noRegion>Newcastle upon Tyne</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Burn, D J" sort="Burn, D J" uniqKey="Burn D" first="D J" last="Burn">D J Burn</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2000">2000</date>
<idno type="RBID">pubmed:11009180</idno>
<idno type="pmid">11009180</idno>
<idno type="wicri:Area/PubMed/Corpus">003F25</idno>
<idno type="wicri:Area/PubMed/Curation">003F25</idno>
<idno type="wicri:Area/PubMed/Checkpoint">003E54</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">The pathogenesis of multiple system atrophy: past, present, and future.</title>
<author><name sortKey="Jaros, E" sort="Jaros, E" uniqKey="Jaros E" first="E" last="Jaros">E. Jaros</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Neuropathology, Newcastle General Hospital, Newcastle upon Tyne, UK.</nlm:affiliation>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Department of Neuropathology, Newcastle General Hospital, Newcastle upon Tyne</wicri:regionArea>
<wicri:noRegion>Newcastle upon Tyne</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Burn, D J" sort="Burn, D J" uniqKey="Burn D" first="D J" last="Burn">D J Burn</name>
</author>
</analytic>
<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2000" type="published">2000</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Biological Markers</term>
<term>Brain (metabolism)</term>
<term>Brain (pathology)</term>
<term>Gene Expression Regulation</term>
<term>Genes, Regulator</term>
<term>Humans</term>
<term>Inclusion Bodies (metabolism)</term>
<term>Inclusion Bodies (pathology)</term>
<term>Multiple System Atrophy (classification)</term>
<term>Multiple System Atrophy (etiology)</term>
<term>Multiple System Atrophy (genetics)</term>
<term>Multiple System Atrophy (metabolism)</term>
<term>Multiple System Atrophy (pathology)</term>
<term>Mutation</term>
<term>Nerve Tissue Proteins (genetics)</term>
<term>Nerve Tissue Proteins (metabolism)</term>
<term>Neuregulins (genetics)</term>
<term>Oligodendroglia (metabolism)</term>
<term>Oligodendroglia (pathology)</term>
<term>Polymorphism, Genetic</term>
<term>Synucleins</term>
<term>alpha-Synuclein</term>
<term>tau Proteins (metabolism)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nerve Tissue Proteins</term>
<term>Neuregulins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Nerve Tissue Proteins</term>
<term>tau Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biological Markers</term>
<term>Synucleins</term>
<term>alpha-Synuclein</term>
</keywords>
<keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Multiple System Atrophy</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Multiple System Atrophy</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Multiple System Atrophy</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term>
<term>Inclusion Bodies</term>
<term>Multiple System Atrophy</term>
<term>Oligodendroglia</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term>
<term>Inclusion Bodies</term>
<term>Multiple System Atrophy</term>
<term>Oligodendroglia</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Gene Expression Regulation</term>
<term>Genes, Regulator</term>
<term>Humans</term>
<term>Mutation</term>
<term>Polymorphism, Genetic</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Multiple system atrophy is a sporadic, adult-onset neurodegenerative disease of unknown etiology. The condition may be unique among neurodegenerative diseases by the prominent, if not primary, role played by the oligodendroglial cell in the pathogenetic process. Recent developments in our understanding of multiple system atrophy have included the detection of glial cytoplasmic inclusions and alpha-synuclein accumulation in these inclusions. The latter finding links multiple system atrophy as an "alpha-synucleinopathy" to Parkinson's disease and dementia with Lewy bodies. This article reviews recent important findings of potential relevance to the pathogenesis of multiple system atrophy. We also speculate on areas in which further advances may be made to progress our understanding of this devastating condition.</div>
</front>
</TEI>
<pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">11009180</PMID>
<DateCreated><Year>2001</Year>
<Month>01</Month>
<Day>09</Day>
</DateCreated>
<DateCompleted><Year>2001</Year>
<Month>01</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised><Year>2005</Year>
<Month>11</Month>
<Day>17</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN>
<JournalIssue CitedMedium="Print"><Volume>15</Volume>
<Issue>5</Issue>
<PubDate><Year>2000</Year>
<Month>Sep</Month>
</PubDate>
</JournalIssue>
<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
<ISOAbbreviation>Mov. Disord.</ISOAbbreviation>
</Journal>
<ArticleTitle>The pathogenesis of multiple system atrophy: past, present, and future.</ArticleTitle>
<Pagination><MedlinePgn>784-8</MedlinePgn>
</Pagination>
<Abstract><AbstractText>Multiple system atrophy is a sporadic, adult-onset neurodegenerative disease of unknown etiology. The condition may be unique among neurodegenerative diseases by the prominent, if not primary, role played by the oligodendroglial cell in the pathogenetic process. Recent developments in our understanding of multiple system atrophy have included the detection of glial cytoplasmic inclusions and alpha-synuclein accumulation in these inclusions. The latter finding links multiple system atrophy as an "alpha-synucleinopathy" to Parkinson's disease and dementia with Lewy bodies. This article reviews recent important findings of potential relevance to the pathogenesis of multiple system atrophy. We also speculate on areas in which further advances may be made to progress our understanding of this devastating condition.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jaros</LastName>
<ForeName>E</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Neuropathology, Newcastle General Hospital, Newcastle upon Tyne, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Burn</LastName>
<ForeName>D J</ForeName>
<Initials>DJ</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D016454">Review</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="D015415">Biological Markers</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D009419">Nerve Tissue Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D020880">Neuregulins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C497604">SNCA protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051843">Synucleins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015415">Biological Markers</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName>
<QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D005786">Gene Expression Regulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D005809">Genes, Regulator</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D002479">Inclusion Bodies</DescriptorName>
<QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D019578">Multiple System Atrophy</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000145">classification</QualifierName>
<QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="Y" UI="D009154">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D009419">Nerve Tissue Proteins</DescriptorName>
<QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName>
<QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D020880">Neuregulins</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D009836">Oligodendroglia</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName>
<QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D011110">Polymorphism, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D051843">Synucleins</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D051844">alpha-Synuclein</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName MajorTopicYN="N" UI="D016875">tau Proteins</DescriptorName>
<QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<NumberOfReferences>61</NumberOfReferences>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year>
<Month>9</Month>
<Day>29</Day>
<Hour>11</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2001</Year>
<Month>2</Month>
<Day>28</Day>
<Hour>10</Hour>
<Minute>1</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2000</Year>
<Month>9</Month>
<Day>29</Day>
<Hour>11</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">11009180</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>Royaume-Uni</li>
</country>
</list>
<tree><noCountry><name sortKey="Burn, D J" sort="Burn, D J" uniqKey="Burn D" first="D J" last="Burn">D J Burn</name>
</noCountry>
<country name="Royaume-Uni"><noRegion><name sortKey="Jaros, E" sort="Jaros, E" uniqKey="Jaros E" first="E" last="Jaros">E. Jaros</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PubMed/Checkpoint

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003E54 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 003E54 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    MovDisordV3
   |flux=    PubMed
   |étape=   Checkpoint
   |type=    RBID
   |clé=     pubmed:11009180
   |texte=   The pathogenesis of multiple system atrophy: past, present, and future.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i   -Sk "pubmed:11009180" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd   \
       | NlmPubMed2Wicri -a MovDisordV3

This area was generated with Dilib version V0.6.23.
Data generation: Sun Jul 3 12:29:32 2016. Site generation: Wed Feb 14 10:52:30 2024

	Movement Disorders (revue)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Movement Disorders (revue)

The pathogenesis of multiple system atrophy: past, present, and future.

The pathogenesis of multiple system atrophy: past, present, and future.

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki