The pathogenesis of multiple system atrophy: past, present, and future.
Identifieur interne : 000326 ( Ncbi/Curation ); précédent : 000325; suivant : 000327The pathogenesis of multiple system atrophy: past, present, and future.
Auteurs : E. Jaros [Royaume-Uni] ; D J BurnSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2000.
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
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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><idno type="wicri:Area/Ncbi/Merge">000326</idno><idno type="wicri:Area/Ncbi/Curation">000326</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></record>Pour manipuler ce document sous Unix (Dilib)
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