Levels of alpha‐synuclein mRNA in sporadic Parkinson disease patients
Identifieur interne : 000905 ( Main/Corpus ); précédent : 000904; suivant : 000906Levels of alpha‐synuclein mRNA in sporadic Parkinson disease patients
Auteurs : Ornit Chiba-Falek ; Grisel J. Lopez ; Robert L. NussbaumSource :
- Movement Disorders [ 0885-3185 ] ; 2006-10.
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- KwdEn :
Abstract
Lewy bodies, the pathological hallmark of Parkinson's disease (PD), consist largely of α‐synuclein, a 14.5‐kDa presynaptic neuronal protein implicated in familial PD. An increased copy number and elevated expression of wild‐type α‐synuclein (SNCA) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of SNCA‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state SNCA‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the SNCA‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. SNCA‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. These results suggest that elevated expression levels of SNCA‐mRNA are found in the affected regions of PD brain and support the hypothesis that increases in α‐synuclein expression is associated, among other factors, with the development of sporadic PD. © 2006 Movement Disorder Society
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DOI: 10.1002/mds.21007
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ISTEX:D44FBB6838A753D6BC7D3B500EADA6EB9762C014Le document en format XML
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An increased copy number and elevated expression of wild‐type α‐synuclein (SNCA) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of SNCA‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state SNCA‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the SNCA‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. SNCA‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. These results suggest that elevated expression levels of SNCA‐mRNA are found in the affected regions of PD brain and support the hypothesis that increases in α‐synuclein expression is associated, among other factors, with the development of sporadic PD. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ornit Chiba‐Falek PhD</name><affiliations><json:string>Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Grisel J. Lopez MD</name><affiliations><json:string>Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Robert L. Nussbaum MD</name><affiliations><json:string>Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>alpha‐synuclein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SNCA‐mRNA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>real‐time PCR</value></json:item></subject><articleId><json:string>MDS21007</json:string></articleId><language><json:string>eng</json:string></language><abstract>Lewy bodies, the pathological hallmark of Parkinson's disease (PD), consist largely of α‐synuclein, a 14.5‐kDa presynaptic neuronal protein implicated in familial PD. An increased copy number and elevated expression of wild‐type α‐synuclein (SNCA) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of SNCA‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state SNCA‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the SNCA‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. SNCA‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2006-10"></date><biblScope unit="volume">21</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1703">1703</biblScope><biblScope unit="page" to="1708">1708</biblScope></imprint></monogr><idno type="istex">D44FBB6838A753D6BC7D3B500EADA6EB9762C014</idno><idno type="DOI">10.1002/mds.21007</idno><idno type="ArticleID">MDS21007</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Lewy bodies, the pathological hallmark of Parkinson's disease (PD), consist largely of α‐synuclein, a 14.5‐kDa presynaptic neuronal protein implicated in familial PD. An increased copy number and elevated expression of wild‐type α‐synuclein (SNCA) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of SNCA‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state SNCA‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the SNCA‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. SNCA‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. These results suggest that elevated expression levels of SNCA‐mRNA are found in the affected regions of PD brain and support the hypothesis that increases in α‐synuclein expression is associated, among other factors, with the development of sporadic PD. © 2006 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>alpha‐synuclein</term></item><item><term>Parkinson disease</term></item><item><term>SNCA‐mRNA</term></item><item><term>real‐time PCR</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-12-06">Received</change><change when="2006-03-13">Registration</change><change when="2006-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D44FBB6838A753D6BC7D3B500EADA6EB9762C014/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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An increased copy number and elevated expression of wild‐type α‐synuclein (<i>SNCA</i>) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of <i>SNCA</i>‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state <i>SNCA</i>‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the <i>SNCA</i>‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. <i>SNCA</i>‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. These results suggest that elevated expression levels of <i>SNCA</i>‐mRNA are found in the affected regions of PD brain and support the hypothesis that increases in α‐synuclein expression is associated, among other factors, with the development of sporadic PD. © 2006 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Levels of alpha‐synuclein mRNA in sporadic Parkinson disease patients</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SNCA‐mRNA Levels in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levels of alpha‐synuclein mRNA in sporadic Parkinson disease patients</title></titleInfo><name type="personal"><namePart type="given">Ornit</namePart><namePart type="family">Chiba‐Falek</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Grisel J.</namePart><namePart type="family">Lopez</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert L.</namePart><namePart type="family">Nussbaum</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA</affiliation><description>Correspondence: Genetic Disease Research Branch, National Human Genome Research Institute, NIH, 49 Convent Drive MSC 4472, Bethesda, MD 20892</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2006-10</dateIssued><dateCaptured encoding="w3cdtf">2005-12-06</dateCaptured><dateValid encoding="w3cdtf">2006-03-13</dateValid><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">2</extent><extent unit="references">20</extent><extent unit="words">3922</extent></physicalDescription><abstract lang="en">Lewy bodies, the pathological hallmark of Parkinson's disease (PD), consist largely of α‐synuclein, a 14.5‐kDa presynaptic neuronal protein implicated in familial PD. An increased copy number and elevated expression of wild‐type α‐synuclein (SNCA) has been shown to cause early‐onset familial PD. However, it is not clear whether increased α‐synuclein expression also plays a role in the pathogenesis of sporadic disease. In the current study, we analyzed the levels of SNCA‐mRNA in affected brains of sporadic PD patients. We compared the levels of steady state SNCA‐mRNA in 7 sporadic PD brain samples and 7 normal controls using real‐time polymerase chain reaction of RNA extracted from mid‐brain tissue, including the substantia nigra. Despite that there is neuronal loss in the substantia nigra of PD brains, overall the SNCA‐mRNA levels were increased in PD brains an average of nearly fourfold over normal control mid‐brain, although there was much greater variability in samples from PD patients compared to controls. Frontal cortex samples from selected individuals were also analyzed. SNCA‐mRNA levels were not significantly changed in PD frontal cortex compared to controls. These results suggest that elevated expression levels of SNCA‐mRNA are found in the affected regions of PD brain and support the hypothesis that increases in α‐synuclein expression is associated, among other factors, with the development of sporadic PD. © 2006 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>alpha‐synuclein</topic><topic>Parkinson disease</topic><topic>SNCA‐mRNA</topic><topic>real‐time PCR</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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