MovDisordV3, PubMed, Corpus, bibRecord, 000131

No evidence for substrate accumulation in Parkinson brains with GBA mutations.

Identifieur interne : 000131 ( PubMed/Corpus ); précédent : 000130; suivant : 000132

No evidence for substrate accumulation in Parkinson brains with GBA mutations.

Auteurs : Matthew E. Gegg ; Lindsay Sweet ; Bing H. Wang ; Lamya S. Shihabuddin ; Sergio Pablo Sardi ; Anthony H V. Schapira

Source :

Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2015.

RBID : pubmed:26096906

Abstract

To establish whether Parkinson's disease (PD) brains previously described to have decreased glucocerebrosidase activity exhibit accumulation of the lysosomal enzyme's substrate, glucosylceramide, or other changes in lipid composition.

DOI: 10.1002/mds.26278
PubMed: 26096906

Links to Exploration step

pubmed:26096906

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">No evidence for substrate accumulation in Parkinson brains with GBA mutations.</title>
<author><name sortKey="Gegg, Matthew E" sort="Gegg, Matthew E" uniqKey="Gegg M" first="Matthew E" last="Gegg">Matthew E. Gegg</name>
<affiliation><nlm:affiliation>Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Sweet, Lindsay" sort="Sweet, Lindsay" uniqKey="Sweet L" first="Lindsay" last="Sweet">Lindsay Sweet</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Wang, Bing H" sort="Wang, Bing H" uniqKey="Wang B" first="Bing H" last="Wang">Bing H. Wang</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Shihabuddin, Lamya S" sort="Shihabuddin, Lamya S" uniqKey="Shihabuddin L" first="Lamya S" last="Shihabuddin">Lamya S. Shihabuddin</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Sardi, Sergio Pablo" sort="Sardi, Sergio Pablo" uniqKey="Sardi S" first="Sergio Pablo" last="Sardi">Sergio Pablo Sardi</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Schapira, Anthony H V" sort="Schapira, Anthony H V" uniqKey="Schapira A" first="Anthony H V" last="Schapira">Anthony H V. Schapira</name>
<affiliation><nlm:affiliation>Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK.</nlm:affiliation>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2015">2015</date>
<idno type="RBID">pubmed:26096906</idno>
<idno type="pmid">26096906</idno>
<idno type="doi">10.1002/mds.26278</idno>
<idno type="wicri:Area/PubMed/Corpus">000131</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">No evidence for substrate accumulation in Parkinson brains with GBA mutations.</title>
<author><name sortKey="Gegg, Matthew E" sort="Gegg, Matthew E" uniqKey="Gegg M" first="Matthew E" last="Gegg">Matthew E. Gegg</name>
<affiliation><nlm:affiliation>Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Sweet, Lindsay" sort="Sweet, Lindsay" uniqKey="Sweet L" first="Lindsay" last="Sweet">Lindsay Sweet</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Wang, Bing H" sort="Wang, Bing H" uniqKey="Wang B" first="Bing H" last="Wang">Bing H. Wang</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Shihabuddin, Lamya S" sort="Shihabuddin, Lamya S" uniqKey="Shihabuddin L" first="Lamya S" last="Shihabuddin">Lamya S. Shihabuddin</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Sardi, Sergio Pablo" sort="Sardi, Sergio Pablo" uniqKey="Sardi S" first="Sergio Pablo" last="Sardi">Sergio Pablo Sardi</name>
<affiliation><nlm:affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Schapira, Anthony H V" sort="Schapira, Anthony H V" uniqKey="Schapira A" first="Anthony H V" last="Schapira">Anthony H V. Schapira</name>
<affiliation><nlm:affiliation>Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK.</nlm:affiliation>
</affiliation>
</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="2015" type="published">2015</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">To establish whether Parkinson's disease (PD) brains previously described to have decreased glucocerebrosidase activity exhibit accumulation of the lysosomal enzyme's substrate, glucosylceramide, or other changes in lipid composition.</div>
</front>
</TEI>
<pubmed><MedlineCitation Owner="NLM" Status="In-Process"><PMID Version="1">26096906</PMID>
<DateCreated><Year>2015</Year>
<Month>07</Month>
<Day>16</Day>
</DateCreated>
<DateRevised><Year>2015</Year>
<Month>08</Month>
<Day>09</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>30</Volume>
<Issue>8</Issue>
<PubDate><Year>2015</Year>
<Month>Jul</Month>
</PubDate>
</JournalIssue>
<Title>Movement disorders : official journal of the Movement Disorder Society</Title>
<ISOAbbreviation>Mov. Disord.</ISOAbbreviation>
</Journal>
<ArticleTitle>No evidence for substrate accumulation in Parkinson brains with GBA mutations.</ArticleTitle>
<Pagination><MedlinePgn>1085-9</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.26278</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">To establish whether Parkinson's disease (PD) brains previously described to have decreased glucocerebrosidase activity exhibit accumulation of the lysosomal enzyme's substrate, glucosylceramide, or other changes in lipid composition.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Lipidomic analyses and cholesterol measurements were performed on the putamen (n = 5-7) and cerebellum (n = 7-14) of controls, Parkinson's disease brains with heterozygote GBA1 mutations (PD+GBA), or sporadic PD.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Total glucosylceramide levels were unchanged in both PD+GBA and sporadic PD brains when compared with controls. No changes in glucosylsphingosine (deacetylated glucosylceramide), sphingomyelin, gangliosides (GM2, GM3), or total cholesterol were observed in either putamen or cerebellum.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">This study did not demonstrate glucocerebrosidase substrate accumulation in PD brains with heterozygote GBA1 mutations in areas of the brain with low α-synuclein pathology.</AbstractText>
<CopyrightInformation>© 2015 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gegg</LastName>
<ForeName>Matthew E</ForeName>
<Initials>ME</Initials>
<AffiliationInfo><Affiliation>Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sweet</LastName>
<ForeName>Lindsay</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Bing H</ForeName>
<Initials>BH</Initials>
<AffiliationInfo><Affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shihabuddin</LastName>
<ForeName>Lamya S</ForeName>
<Initials>LS</Initials>
<AffiliationInfo><Affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sardi</LastName>
<ForeName>Sergio Pablo</ForeName>
<Initials>SP</Initials>
<AffiliationInfo><Affiliation>Genzyme, a Sanofi Company, Framingham, Massachusetts, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schapira</LastName>
<ForeName>Anthony H V</ForeName>
<Initials>AH</Initials>
<AffiliationInfo><Affiliation>Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>089698</GrantID>
<Agency>Wellcome Trust</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><GrantID>MR/L501499/1</GrantID>
<Agency>Medical Research Council</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><GrantID>WT089698</GrantID>
<Agency>Wellcome Trust</Agency>
<Country>United Kingdom</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2015</Year>
<Month>06</Month>
<Day>11</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Mov Disord</MedlineTA>
<NlmUniqueID>8610688</NlmUniqueID>
<ISSNLinking>0885-3185</ISSNLinking>
</MedlineJournalInfo>
<CitationSubset>IM</CitationSubset>
<CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2012 Mar 20;109(12):E705-14</RefSource>
<PMID Version="1">22331875</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Commun. 2014;5:4028</RefSource>
<PMID Version="1">24905578</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Hum Mutat. 2004 Jun;23(6):567-75</RefSource>
<PMID Version="1">15146461</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 1982 Sep;39(3):709-18</RefSource>
<PMID Version="1">7097276</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Clin Genet. 1985 May;27(5):443-50</RefSource>
<PMID Version="1">3924448</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 1999 Mar;103(6):817-23</RefSource>
<PMID Version="1">10079102</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>EMBO J. 2006 Sep 6;25(17):3921-33</RefSource>
<PMID Version="1">16917501</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Lancet. 2008 Oct 4;372(9645):1263-71</RefSource>
<PMID Version="1">19094956</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Brain. 2009 Jul;132(Pt 7):1783-94</RefSource>
<PMID Version="1">19286695</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>N Engl J Med. 2009 Oct 22;361(17):1651-61</RefSource>
<PMID Version="1">19846850</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2010 Aug;24(8):3052-65</RefSource>
<PMID Version="1">20375270</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2010 Sep 15;30(37):12535-44</RefSource>
<PMID Version="1">20844148</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2010 Dec;67(12):1464-72</RefSource>
<PMID Version="1">20697033</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Autophagy. 2011 Feb;7(2):243-5</RefSource>
<PMID Version="1">21139416</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2011 Jun;69(6):940-53</RefSource>
<PMID Version="1">21472771</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell. 2011 Jul 8;146(1):37-52</RefSource>
<PMID Version="1">21700325</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2011 Jul 19;108(29):12101-6</RefSource>
<PMID Version="1">21730160</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Med. 2011 Sep-Oct;17(9-10):1107-18</RefSource>
<PMID Version="1">21717034</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Genet Metab. 2012 Mar;105(3):528-9</RefSource>
<PMID Version="1">22227325</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Neurology. 2012 Jul 17;79(3):213-20</RefSource>
<PMID Version="1">22722629</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2012 Sep;72(3):455-63</RefSource>
<PMID Version="1">23034917</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2013 Feb;28(2):232-6</RefSource>
<PMID Version="1">23225227</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2013;8(3):e57560</RefSource>
<PMID Version="1">23520473</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cell Metab. 2013 Jun 4;17(6):941-53</RefSource>
<PMID Version="1">23707074</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nat Rev Mol Cell Biol. 2013 Dec;14(12):759-74</RefSource>
<PMID Version="1">24201109</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Brain. 2014 Mar;137(Pt 3):834-48</RefSource>
<PMID Version="1">24477431</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Brain. 2014 May;137(Pt 5):1481-95</RefSource>
<PMID Version="1">24574503</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2014 Apr;29(4):518-26</RefSource>
<PMID Version="1">24822250</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Genet Metab. 2002 Aug;76(4):262-70</RefSource>
<PMID Version="1">12208131</PMID>
</CommentsCorrections>
</CommentsCorrectionsList>
<OtherID Source="NLM">EMS64556</OtherID>
<OtherID Source="NLM">PMC4529481</OtherID>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Parkinson's disease</Keyword>
<Keyword MajorTopicYN="N">glucocerebrosidase</Keyword>
<Keyword MajorTopicYN="N">lysosomes</Keyword>
<Keyword MajorTopicYN="N">sphingolipids</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year>
<Month>1</Month>
<Day>14</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2015</Year>
<Month>4</Month>
<Day>20</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2015</Year>
<Month>5</Month>
<Day>3</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="aheadofprint"><Year>2015</Year>
<Month>6</Month>
<Day>11</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2015</Year>
<Month>6</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2015</Year>
<Month>6</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2015</Year>
<Month>6</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">26096906</ArticleId>
<ArticleId IdType="doi">10.1002/mds.26278</ArticleId>
<ArticleId IdType="pmc">PMC4529481</ArticleId>
<ArticleId IdType="mid">EMS64556</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>

Pour manipuler ce document sous Unix (Dilib)

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

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000131 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 000131 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Wicri/Santé
   |area=    MovDisordV3
   |flux=    PubMed
   |étape=   Corpus
   |type=    RBID
   |clé=     pubmed:26096906
   |texte=   No evidence for substrate accumulation in Parkinson brains with GBA mutations.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i   -Sk "pubmed:26096906" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/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)

No evidence for substrate accumulation in Parkinson brains with GBA mutations.

No evidence for substrate accumulation in Parkinson brains with GBA mutations.

Source :

Abstract

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