Multiple system atrophy: a prototypical synucleinopathy for disease-modifying therapeutic strategies.
Identifieur interne : 000542 ( PubMed/Corpus ); précédent : 000541; suivant : 000543Multiple system atrophy: a prototypical synucleinopathy for disease-modifying therapeutic strategies.
Auteurs : Pierre-Olivier Fernagut ; Benjamin Dehay ; Aline Maillard ; Erwan Bezard ; Paul Perez ; Anne Pavy-Le Traon ; Olivier Rascol ; Alexandra Foubert-Samier ; François Tison ; Wassilios G. MeissnerSource :
- Neurobiology of disease [ 1095-953X ] ; 2014.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : alpha-Synuclein.
- metabolism : Brain, Multiple System Atrophy.
- pathology : Multiple System Atrophy.
- therapy : Multiple System Atrophy, Parkinson Disease.
- Clinical Trials as Topic, Humans.
Abstract
Despite active fundamental, translational and clinical research, no therapeutic intervention has yet shown convincing effects on disease progression in Parkinson's disease (PD) patients. Indeed, several disease-modification trials failed or proved to be inconclusive due to lack of consistency between clinical rating scales and putative surrogate markers of disease progression, or confounding symptomatic effects of the tested compound. Multiple system atrophy (MSA) is a rapidly progressing orphan disorder leading to severe motor disability within a few years. Together with PD and dementia with Lewy bodies (DLB), MSA belongs to the synucleinopathies, a group of neurodegenerative disorders characterized by the abnormal accumulation of alpha-synuclein. Crucial milestones have been reached for successfully conducting clinical intervention trials in a large number of patients with MSA. In this personal view, we will review evidence, and discuss why MSA could prove the most relevant clinical model for assessing treatments that target mechanisms operating in all synucleinopathies.
DOI: 10.1016/j.nbd.2014.03.021
PubMed: 24727096
Links to Exploration step
pubmed:24727096Le document en format XML
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Meissner</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France; Centre de référence atrophie multisystématisée, CHU de Bordeaux, Pessac, France. Electronic address: wassilios.meissner@chu-bordeaux.fr.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24727096</idno><idno type="pmid">24727096</idno><idno type="doi">10.1016/j.nbd.2014.03.021</idno><idno type="wicri:Area/PubMed/Corpus">000542</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000542</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Multiple system atrophy: a prototypical synucleinopathy for disease-modifying therapeutic strategies.</title><author><name sortKey="Fernagut, Pierre Olivier" sort="Fernagut, Pierre Olivier" uniqKey="Fernagut P" first="Pierre-Olivier" last="Fernagut">Pierre-Olivier Fernagut</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.</nlm:affiliation></affiliation></author><author><name sortKey="Dehay, Benjamin" sort="Dehay, Benjamin" uniqKey="Dehay B" first="Benjamin" last="Dehay">Benjamin Dehay</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.</nlm:affiliation></affiliation></author><author><name sortKey="Maillard, Aline" sort="Maillard, Aline" uniqKey="Maillard A" first="Aline" last="Maillard">Aline Maillard</name><affiliation><nlm:affiliation>CHU de Bordeaux, Unité de Soutien Méthodologique à la Recherche Clinique (USMR), Pôle de santé publique, Bordeaux, France.</nlm:affiliation></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France.</nlm:affiliation></affiliation></author><author><name sortKey="Perez, Paul" sort="Perez, Paul" uniqKey="Perez P" first="Paul" last="Perez">Paul Perez</name><affiliation><nlm:affiliation>CHU de Bordeaux, Unité de Soutien Méthodologique à la Recherche Clinique (USMR), Pôle de santé publique, Bordeaux, France.</nlm:affiliation></affiliation></author><author><name sortKey="Pavy Le Traon, Anne" sort="Pavy Le Traon, Anne" uniqKey="Pavy Le Traon A" first="Anne" last="Pavy-Le Traon">Anne Pavy-Le Traon</name><affiliation><nlm:affiliation>Centre de référence atrophie multisystématisée, CHU de Toulouse, Toulouse, France.</nlm:affiliation></affiliation></author><author><name sortKey="Rascol, Olivier" sort="Rascol, Olivier" uniqKey="Rascol O" first="Olivier" last="Rascol">Olivier Rascol</name><affiliation><nlm:affiliation>Centre de référence atrophie multisystématisée, CHU de Toulouse, Toulouse, France; Department of Clinical Pharmacology, University Hospital and University of Toulouse 3, Toulouse, France; Department of Neurosciences, University Hospital and University of Toulouse 3, Toulouse, France; INSERM UMR825 and CIC9302, Toulouse, France.</nlm:affiliation></affiliation></author><author><name sortKey="Foubert Samier, Alexandra" sort="Foubert Samier, Alexandra" uniqKey="Foubert Samier A" first="Alexandra" last="Foubert-Samier">Alexandra Foubert-Samier</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France; Centre de référence atrophie multisystématisée, CHU de Bordeaux, Pessac, France.</nlm:affiliation></affiliation></author><author><name sortKey="Tison, Francois" sort="Tison, Francois" uniqKey="Tison F" first="François" last="Tison">François Tison</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France; Centre de référence atrophie multisystématisée, CHU de Bordeaux, Pessac, France.</nlm:affiliation></affiliation></author><author><name sortKey="Meissner, Wassilios G" sort="Meissner, Wassilios G" uniqKey="Meissner W" first="Wassilios G" last="Meissner">Wassilios G. Meissner</name><affiliation><nlm:affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France; Centre de référence atrophie multisystématisée, CHU de Bordeaux, Pessac, France. Electronic address: wassilios.meissner@chu-bordeaux.fr.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Neurobiology of disease</title><idno type="eISSN">1095-953X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Brain (metabolism)</term><term>Clinical Trials as Topic</term><term>Humans</term><term>Multiple System Atrophy (metabolism)</term><term>Multiple System Atrophy (pathology)</term><term>Multiple System Atrophy (therapy)</term><term>Parkinson Disease (therapy)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Multiple System Atrophy</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Clinical Trials as Topic</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Despite active fundamental, translational and clinical research, no therapeutic intervention has yet shown convincing effects on disease progression in Parkinson's disease (PD) patients. Indeed, several disease-modification trials failed or proved to be inconclusive due to lack of consistency between clinical rating scales and putative surrogate markers of disease progression, or confounding symptomatic effects of the tested compound. Multiple system atrophy (MSA) is a rapidly progressing orphan disorder leading to severe motor disability within a few years. Together with PD and dementia with Lewy bodies (DLB), MSA belongs to the synucleinopathies, a group of neurodegenerative disorders characterized by the abnormal accumulation of alpha-synuclein. Crucial milestones have been reached for successfully conducting clinical intervention trials in a large number of patients with MSA. In this personal view, we will review evidence, and discuss why MSA could prove the most relevant clinical model for assessing treatments that target mechanisms operating in all synucleinopathies.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24727096</PMID><DateCreated><Year>2014</Year><Month>05</Month><Day>26</Day></DateCreated><DateCompleted><Year>2015</Year><Month>01</Month><Day>06</Day></DateCompleted><DateRevised><Year>2014</Year><Month>05</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-953X</ISSN><JournalIssue CitedMedium="Internet"><Volume>67</Volume><PubDate><Year>2014</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Neurobiology of disease</Title><ISOAbbreviation>Neurobiol. Dis.</ISOAbbreviation></Journal><ArticleTitle>Multiple system atrophy: a prototypical synucleinopathy for disease-modifying therapeutic strategies.</ArticleTitle><Pagination><MedlinePgn>133-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.nbd.2014.03.021</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0969-9961(14)00082-5</ELocationID><Abstract><AbstractText>Despite active fundamental, translational and clinical research, no therapeutic intervention has yet shown convincing effects on disease progression in Parkinson's disease (PD) patients. Indeed, several disease-modification trials failed or proved to be inconclusive due to lack of consistency between clinical rating scales and putative surrogate markers of disease progression, or confounding symptomatic effects of the tested compound. Multiple system atrophy (MSA) is a rapidly progressing orphan disorder leading to severe motor disability within a few years. Together with PD and dementia with Lewy bodies (DLB), MSA belongs to the synucleinopathies, a group of neurodegenerative disorders characterized by the abnormal accumulation of alpha-synuclein. Crucial milestones have been reached for successfully conducting clinical intervention trials in a large number of patients with MSA. In this personal view, we will review evidence, and discuss why MSA could prove the most relevant clinical model for assessing treatments that target mechanisms operating in all synucleinopathies.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fernagut</LastName><ForeName>Pierre-Olivier</ForeName><Initials>PO</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dehay</LastName><ForeName>Benjamin</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maillard</LastName><ForeName>Aline</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>CHU de Bordeaux, Unité de Soutien Méthodologique à la Recherche Clinique (USMR), Pôle de santé publique, Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>Erwan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Perez</LastName><ForeName>Paul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>CHU de Bordeaux, Unité de Soutien Méthodologique à la Recherche Clinique (USMR), Pôle de santé publique, Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pavy-Le Traon</LastName><ForeName>Anne</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Centre de référence atrophie multisystématisée, CHU de Toulouse, Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rascol</LastName><ForeName>Olivier</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Centre de référence atrophie multisystématisée, CHU de Toulouse, Toulouse, France; Department of Clinical Pharmacology, University Hospital and University of Toulouse 3, Toulouse, France; Department of Neurosciences, University Hospital and University of Toulouse 3, Toulouse, France; INSERM UMR825 and CIC9302, Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Foubert-Samier</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France; Centre de référence atrophie multisystématisée, CHU de Bordeaux, Pessac, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tison</LastName><ForeName>François</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France; Centre de référence atrophie multisystématisée, CHU de Bordeaux, Pessac, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meissner</LastName><ForeName>Wassilios G</ForeName><Initials>WG</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000 Bordeaux, France; Service de Neurologie, CHU de Bordeaux, F-33604 Pessac, France; Centre de référence atrophie multisystématisée, CHU de Bordeaux, Pessac, France. Electronic address: wassilios.meissner@chu-bordeaux.fr.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>04</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neurobiol Dis</MedlineTA><NlmUniqueID>9500169</NlmUniqueID><ISSNLinking>0969-9961</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002986" MajorTopicYN="N">Clinical Trials as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019578" MajorTopicYN="N">Multiple System Atrophy</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051844" MajorTopicYN="N">alpha-Synuclein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alpha-synuclein</Keyword><Keyword MajorTopicYN="N">Disease-modifying</Keyword><Keyword MajorTopicYN="N">Multiple system atrophy</Keyword><Keyword MajorTopicYN="N">Synucleinopathies</Keyword><Keyword MajorTopicYN="N">Therapeutic strategies</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>02</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>03</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>03</Month><Day>31</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>4</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>4</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>1</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24727096</ArticleId><ArticleId IdType="pii">S0969-9961(14)00082-5</ArticleId><ArticleId IdType="doi">10.1016/j.nbd.2014.03.021</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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