α-Synuclein in Parkinson disease and other neurodegenerative disorders
Identifieur interne : 000415 ( Main/Corpus ); précédent : 000414; suivant : 000416α-Synuclein in Parkinson disease and other neurodegenerative disorders
Auteurs : Michael Eller ; David R. WilliamsSource :
- Clinical Chemistry and Laboratory Medicine [ 1434-6621 ] ; 2011-03-01.
Abstract
With the aging population in the Western hemisphere, neurodegenerative parkinsonism and dementia will become two of the great public health challenges of this century. A major pillar in the effort to treat these conditions will be the shift from symptomatic treatment to disease modifying therapy. This step will absolutely require cheap and reliable biomarkers; patients will need to be diagnosed before irreversible change has occurred. α-Synuclein (αS) is a recent candidate biomarker for Lewy body neurodegeneration. It is a 140 amino acid protein that forms the pathological substrate in idiopathic Parkinson's disease (IPD), dementia with Lewy bodies (DLB), as well as multiple system atrophy (MSA), a group of disorders collectively known as the synucleopathies. Biomarker research has investigated αS in blood, skin and cerebrospinal fluid (CSF). Plasma assays have demonstrated inconsistent results but CSF assays show a higher degree of uniformity, mostly demonstrating lower levels of αS in patients with Lewy body disease compared to controls. These results are not yet accurate or reliable enough to use as screening tools or isolated diagnostic tests in established disease. It has become clear that factors other than neurodegeneration affect αS concentrations in these tissue samples, such as genetic and environmental influences. Future studies using standardized techniques and larger patient numbers are awaited to realise the full potential of αS as a more definitive diagnostic biomarker.
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DOI: 10.1515/CCLM.2011.077
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Williams</name></author></analytic><monogr></monogr><series><title level="j">Clinical Chemistry and Laboratory Medicine</title><idno type="ISSN">1434-6621</idno><idno type="eISSN">1437-4331</idno><imprint><publisher>Walter de Gruyter</publisher><date type="published" when="2011-03-01">2011-03-01</date><biblScope unit="volume">49</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="403">403</biblScope><biblScope unit="page" to="408">408</biblScope></imprint><idno type="ISSN">1434-6621</idno></series><idno type="istex">98E617BE975E9B0DE8CB46F22667C9BE3608A453</idno><idno type="DOI">10.1515/CCLM.2011.077</idno><idno type="ArticleID">cclm.2011.077</idno><idno type="Related-article-Href">cclm.2011.077.pdf</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1434-6621</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">With the aging population in the Western hemisphere, neurodegenerative parkinsonism and dementia will become two of the great public health challenges of this century. A major pillar in the effort to treat these conditions will be the shift from symptomatic treatment to disease modifying therapy. This step will absolutely require cheap and reliable biomarkers; patients will need to be diagnosed before irreversible change has occurred. α-Synuclein (αS) is a recent candidate biomarker for Lewy body neurodegeneration. It is a 140 amino acid protein that forms the pathological substrate in idiopathic Parkinson's disease (IPD), dementia with Lewy bodies (DLB), as well as multiple system atrophy (MSA), a group of disorders collectively known as the synucleopathies. Biomarker research has investigated αS in blood, skin and cerebrospinal fluid (CSF). Plasma assays have demonstrated inconsistent results but CSF assays show a higher degree of uniformity, mostly demonstrating lower levels of αS in patients with Lewy body disease compared to controls. These results are not yet accurate or reliable enough to use as screening tools or isolated diagnostic tests in established disease. It has become clear that factors other than neurodegeneration affect αS concentrations in these tissue samples, such as genetic and environmental influences. Future studies using standardized techniques and larger patient numbers are awaited to realise the full potential of αS as a more definitive diagnostic biomarker.</div></front></TEI><istex><corpusName>degruyter-journals</corpusName><author><json:item><name>Michael Eller</name><affiliations><json:string>Department of Neurosciences, Alfred Hospital, Melbourne, Australia</json:string></affiliations></json:item><json:item><name>David R. 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These results are not yet accurate or reliable enough to use as screening tools or isolated diagnostic tests in established disease. It has become clear that factors other than neurodegeneration affect αS concentrations in these tissue samples, such as genetic and environmental influences. Future studies using standardized techniques and larger patient numbers are awaited to realise the full potential of αS as a more definitive diagnostic biomarker.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>α-synuclein</term></item><item><term>dementia with Lewy bodies</term></item><item><term>multiple system atrophy</term></item><item><term>Parkinson's disease</term></item><item><term>synucleopathy</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-02-23">Created</change><change when="2011-03-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-13">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/98E617BE975E9B0DE8CB46F22667C9BE3608A453/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus degruyter-journals" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Atypon//DTD Atypon Systems Journal Archiving and Interchange NLM DTD v3.0.2 20101108//EN" URI="atypon_archive-interchange-dtd-3.0.2/atypon-archivearticle3.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="review-article" xml:lang="EN"><front><journal-meta><journal-id journal-id-type="publisher-id">cclm</journal-id><journal-title-group><abbrev-journal-title abbrev-type="full">Clinical Chemistry and Laboratory Medicine</abbrev-journal-title></journal-title-group><issn pub-type="epub">1437-4331</issn><issn pub-type="ppub">1434-6621</issn><publisher><publisher-name>Walter de Gruyter</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">cclm.2011.077</article-id><article-id pub-id-type="doi">10.1515/CCLM.2011.077</article-id><article-categories><subj-group subj-group-type="heading"><subject>Reviews</subject></subj-group></article-categories><title-group><article-title>α-Synuclein in Parkinson disease and other neurodegenerative disorders</article-title></title-group><contrib-group><contrib contrib-type="author"><name name-style="western"><surname>Eller</surname><given-names>Michael</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><x>, </x></contrib><contrib contrib-type="author"><name name-style="western"><surname>Williams</surname><given-names>David R.</given-names></name><email>david.williams@monash.edu</email><xref ref-type="aff" rid="aff1 aff2"><sup>1,2</sup></xref><x>, </x></contrib><aff id="aff1"><sup>1</sup>Department of Neurosciences, Alfred Hospital, Melbourne, Australia</aff><aff id="aff2"><sup>2</sup>Van Cleef Roet Centre for Nervous Diseases, Monash University, Melbourne, Australia</aff></contrib-group><author-notes><corresp>Corresponding author: A/Prof. David R. Williams, Van Cleef Roet Centre for Nervous Diseases, Monash University, Commercial Road, Melbourne 3004, Australia Phone: +61 90765231, Fax: +61 3 90762671</corresp></author-notes><pub-date pub-type="ppub"><day>01</day><month>03</month><year>2011</year><string-date>March 2011</string-date></pub-date><pub-date pub-type="epub"><day>23</day><month>02</month><year>2011</year></pub-date><volume>49</volume><issue>3</issue><fpage>403</fpage><lpage>408</lpage><history><date date-type="received"><day>3</day><month>9</month><year>2010</year></date><date date-type="accepted"><day>21</day><month>11</month><year>2010;</year></date></history><permissions><copyright-statement>©2011 by Walter de Gruyter Berlin New York</copyright-statement><copyright-year>2011</copyright-year></permissions><related-article related-article-type="pdf" xlink:href="cclm.2011.077.pdf"></related-article><abstract><title>Abstract</title><p>With the aging population in the Western hemisphere, neurodegenerative parkinsonism and dementia will become two of the great public health challenges of this century. A major pillar in the effort to treat these conditions will be the shift from symptomatic treatment to disease modifying therapy. This step will absolutely require cheap and reliable biomarkers; patients will need to be diagnosed before irreversible change has occurred. α-Synuclein (αS) is a recent candidate biomarker for Lewy body neurodegeneration. It is a 140 amino acid protein that forms the pathological substrate in idiopathic Parkinson's disease (IPD), dementia with Lewy bodies (DLB), as well as multiple system atrophy (MSA), a group of disorders collectively known as the synucleopathies. Biomarker research has investigated αS in blood, skin and cerebrospinal fluid (CSF). Plasma assays have demonstrated inconsistent results but CSF assays show a higher degree of uniformity, mostly demonstrating lower levels of αS in patients with Lewy body disease compared to controls. These results are not yet accurate or reliable enough to use as screening tools or isolated diagnostic tests in established disease. It has become clear that factors other than neurodegeneration affect αS concentrations in these tissue samples, such as genetic and environmental influences. Future studies using standardized techniques and larger patient numbers are awaited to realise the full potential of αS as a more definitive diagnostic biomarker.</p></abstract><kwd-group><title>Keywords</title><kwd>α-synuclein</kwd><x>, </x><kwd>dementia with Lewy bodies</kwd><x>, </x><kwd>multiple system atrophy</kwd><x>, </x><kwd>Parkinson's disease</kwd><x>, </x><kwd>synucleopathy</kwd></kwd-group><counts><fig-count count="1"></fig-count><table-count count="1"></table-count><ref-count count="40"></ref-count></counts></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>α-Synuclein in Parkinson disease and other neurodegenerative disorders</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>α-Synuclein in Parkinson disease and other neurodegenerative disorders</title></titleInfo><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Eller</namePart><affiliation>Department of Neurosciences, Alfred Hospital, Melbourne, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David R.</namePart><namePart type="family">Williams</namePart><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article"></genre><originInfo><publisher>Walter de Gruyter</publisher><dateIssued encoding="w3cdtf">2011-03-01</dateIssued><dateCreated encoding="w3cdtf">2011-02-23</dateCreated><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">40</extent></physicalDescription><abstract lang="en">With the aging population in the Western hemisphere, neurodegenerative parkinsonism and dementia will become two of the great public health challenges of this century. A major pillar in the effort to treat these conditions will be the shift from symptomatic treatment to disease modifying therapy. This step will absolutely require cheap and reliable biomarkers; patients will need to be diagnosed before irreversible change has occurred. α-Synuclein (αS) is a recent candidate biomarker for Lewy body neurodegeneration. It is a 140 amino acid protein that forms the pathological substrate in idiopathic Parkinson's disease (IPD), dementia with Lewy bodies (DLB), as well as multiple system atrophy (MSA), a group of disorders collectively known as the synucleopathies. Biomarker research has investigated αS in blood, skin and cerebrospinal fluid (CSF). Plasma assays have demonstrated inconsistent results but CSF assays show a higher degree of uniformity, mostly demonstrating lower levels of αS in patients with Lewy body disease compared to controls. These results are not yet accurate or reliable enough to use as screening tools or isolated diagnostic tests in established disease. It has become clear that factors other than neurodegeneration affect αS concentrations in these tissue samples, such as genetic and environmental influences. Future studies using standardized techniques and larger patient numbers are awaited to realise the full potential of αS as a more definitive diagnostic biomarker.</abstract><note type="author-notes">Corresponding author: A/Prof. David R. Williams, Van Cleef Roet Centre for Nervous Diseases, Monash University, Commercial Road, Melbourne 3004, Australia Phone: +61 90765231, Fax: +61 3 90762671</note><subject><genre>Keywords</genre><topic>α-synuclein</topic><topic>dementia with Lewy bodies</topic><topic>multiple system atrophy</topic><topic>Parkinson's disease</topic><topic>synucleopathy</topic></subject><relatedItem type="host"><titleInfo><title>Clinical Chemistry and Laboratory Medicine</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1434-6621</identifier><identifier type="eISSN">1437-4331</identifier><identifier type="PublisherID">cclm</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>49</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>403</start><end>408</end></extent></part></relatedItem><relatedItem type="reviewOf"><genre>pdf</genre><identifier type="pdf">cclm.2011.077.pdf</identifier></relatedItem><identifier type="istex">98E617BE975E9B0DE8CB46F22667C9BE3608A453</identifier><identifier type="DOI">10.1515/CCLM.2011.077</identifier><identifier type="ArticleID">cclm.2011.077</identifier><identifier type="Related-article-Href">cclm.2011.077.pdf</identifier><accessCondition type="use and reproduction" contentType="copyright">©2011 by Walter de Gruyter Berlin New York</accessCondition><recordInfo><recordContentSource>De Gruyter</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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