Biomarkers for Parkison's disease: Tools to assess Parkinson's disease onset and progression
Identifieur interne : 000108 ( Main/Corpus ); précédent : 000107; suivant : 000109Biomarkers for Parkison's disease: Tools to assess Parkinson's disease onset and progression
Auteurs : Kenneth Marek ; Danna Jennings ; Gilles Tamagnan ; John SeibylSource :
- Annals of Neurology [ 0364-5134 ] ; 2008-12.
Abstract
Reliable and well‐validated biomarkers for PD to identify individuals “at risk” before motor symptoms, accurately diagnose individuals at the threshold of clinical PD, and monitor PD progression throughout its course would dramatically accelerate research into both PD cause and therapeutics. Biomarkers offer the potential to provide a window onto disease mechanism, potentially generating therapeutic targets for disease. In particular, biomarkers enable investigation of the premotor period of PD before typical symptoms are manifest, but while degeneration has already begun. Given the multiple genetic causes for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset and the clear heterogeneity of clinical symptoms in PD onset and clinical progression, it is likely many biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms will be necessary to fully map PD risk and progression. Biomarkers are also critical in new drug development for PD, both in early validation studies to assess drug dosing and to determine drug penetrance into the brain, and in later efficacy studies to complement PD clinical outcomes. During the past two decades, much progress has been made in identifying and assessing PD biomarkers, but as yet, no fully validated biomarker for PD is currently available. Nonetheless, there is increasing evidence that molecular genetics, focused ‐omic (proteomic, metabolomic, and transcriptomic) assessment of blood and cerebrospinal fluid, and advanced in vivo brain imaging will provide critical clues to assist in the diagnosis and medical management of PD patients. Ann Neurol 2008;64 (suppl):S111–S121
Url:
DOI: 10.1002/ana.21602
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ISTEX:0EEFB35A16B0C4B53498468A4125CA19E9BC5EC2Le document en format XML
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Biomarkers offer the potential to provide a window onto disease mechanism, potentially generating therapeutic targets for disease. In particular, biomarkers enable investigation of the premotor period of PD before typical symptoms are manifest, but while degeneration has already begun. Given the multiple genetic causes for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset and the clear heterogeneity of clinical symptoms in PD onset and clinical progression, it is likely many biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms will be necessary to fully map PD risk and progression. Biomarkers are also critical in new drug development for PD, both in early validation studies to assess drug dosing and to determine drug penetrance into the brain, and in later efficacy studies to complement PD clinical outcomes. During the past two decades, much progress has been made in identifying and assessing PD biomarkers, but as yet, no fully validated biomarker for PD is currently available. Nonetheless, there is increasing evidence that molecular genetics, focused ‐omic (proteomic, metabolomic, and transcriptomic) assessment of blood and cerebrospinal fluid, and advanced in vivo brain imaging will provide critical clues to assist in the diagnosis and medical management of PD patients. Ann Neurol 2008;64 (suppl):S111–S121</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Kenneth Marek MD</name><affiliations><json:string>Institute for Neurodegenerative Disorders, New Haven, CT</json:string></affiliations></json:item><json:item><name>Danna Jennings MD</name><affiliations><json:string>Institute for Neurodegenerative Disorders, New Haven, CT</json:string></affiliations></json:item><json:item><name>Gilles Tamagnan PhD</name><affiliations><json:string>Institute for Neurodegenerative Disorders, New Haven, CT</json:string></affiliations></json:item><json:item><name>John Seibyl MD</name><affiliations><json:string>Institute for Neurodegenerative Disorders, New Haven, CT</json:string></affiliations></json:item></author><articleId><json:string>ANA21602</json:string></articleId><language><json:string>eng</json:string></language><abstract>Reliable and well‐validated biomarkers for PD to identify individuals “at risk” before motor symptoms, accurately diagnose individuals at the threshold of clinical PD, and monitor PD progression throughout its course would dramatically accelerate research into both PD cause and therapeutics. Biomarkers offer the potential to provide a window onto disease mechanism, potentially generating therapeutic targets for disease. In particular, biomarkers enable investigation of the premotor period of PD before typical symptoms are manifest, but while degeneration has already begun. Given the multiple genetic causes for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset and the clear heterogeneity of clinical symptoms in PD onset and clinical progression, it is likely many biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms will be necessary to fully map PD risk and progression. Biomarkers are also critical in new drug development for PD, both in early validation studies to assess drug dosing and to determine drug penetrance into the brain, and in later efficacy studies to complement PD clinical outcomes. During the past two decades, much progress has been made in identifying and assessing PD biomarkers, but as yet, no fully validated biomarker for PD is currently available. Nonetheless, there is increasing evidence that molecular genetics, focused ‐omic (proteomic, metabolomic, and transcriptomic) assessment of blood and cerebrospinal fluid, and advanced in vivo brain imaging will provide critical clues to assist in the diagnosis and medical management of PD patients. 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K.M. has served as a consultant for BI, Pfizer, Novartis, GE Health, Alseres, Merck Serono, Lilly, Bayer Schering Pharma, Elan, and has equity interest in Molecular NeuroImaging, LLC. D.J. is a consultant for BI, Genzyme and Teva. D.J. is an employee of Molecular NeuroImaging, LLC. G.T. has no financial interests to disclose. J.P.S. has served as a consultant for BI, Avid Radiopharmaceuticals, Bayer Schering Healthcare, Pfizer, Takeda Pharmaceuticals, Lilly, GE Healthcare, Alseres, Novartis, Eisai, and has equity interest in Molecular Neuroimaging, LLC.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Biomarkers for Parkison's disease: Tools to assess Parkinson's disease onset and progression</title><author><persName><forename type="first">Kenneth</forename><surname>Marek</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Institute for Neurodegenerative Disorders, 60 Temple Street, New Haven, CT 06510</p></note><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation></author><author><persName><forename type="first">Danna</forename><surname>Jennings</surname></persName><roleName type="degree">MD</roleName><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation></author><author><persName><forename type="first">Gilles</forename><surname>Tamagnan</surname></persName><roleName type="degree">PhD</roleName><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation></author><author><persName><forename type="first">John</forename><surname>Seibyl</surname></persName><roleName type="degree">MD</roleName><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2008-12"></date><biblScope unit="volume">64</biblScope><biblScope unit="issue">S2</biblScope><biblScope unit="supplement">2</biblScope><biblScope unit="page" from="S111">S111</biblScope><biblScope unit="page" to="S121">S121</biblScope></imprint></monogr><idno type="istex">0EEFB35A16B0C4B53498468A4125CA19E9BC5EC2</idno><idno type="DOI">10.1002/ana.21602</idno><idno type="ArticleID">ANA21602</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2008</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Reliable and well‐validated biomarkers for PD to identify individuals “at risk” before motor symptoms, accurately diagnose individuals at the threshold of clinical PD, and monitor PD progression throughout its course would dramatically accelerate research into both PD cause and therapeutics. Biomarkers offer the potential to provide a window onto disease mechanism, potentially generating therapeutic targets for disease. In particular, biomarkers enable investigation of the premotor period of PD before typical symptoms are manifest, but while degeneration has already begun. Given the multiple genetic causes for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset and the clear heterogeneity of clinical symptoms in PD onset and clinical progression, it is likely many biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms will be necessary to fully map PD risk and progression. Biomarkers are also critical in new drug development for PD, both in early validation studies to assess drug dosing and to determine drug penetrance into the brain, and in later efficacy studies to complement PD clinical outcomes. During the past two decades, much progress has been made in identifying and assessing PD biomarkers, but as yet, no fully validated biomarker for PD is currently available. Nonetheless, there is increasing evidence that molecular genetics, focused ‐omic (proteomic, metabolomic, and transcriptomic) assessment of blood and cerebrospinal fluid, and advanced in vivo brain imaging will provide critical clues to assist in the diagnosis and medical management of PD patients. 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xml:lang="en">Biomarkers for PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Kenneth</givenNames><familyName>Marek</familyName><degrees>MD</degrees></personName><contactDetails><email>kmarek@indd.org</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Danna</givenNames><familyName>Jennings</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Gilles</givenNames><familyName>Tamagnan</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>John</givenNames><familyName>Seibyl</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Institute for Neurodegenerative Disorders, New Haven, CT</unparsedAffiliation></affiliation></affiliationGroup><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Reliable and well‐validated biomarkers for PD to identify individuals “at risk” before motor symptoms, accurately diagnose individuals at the threshold of clinical PD, and monitor PD progression throughout its course would dramatically accelerate research into both PD cause and therapeutics. Biomarkers offer the potential to provide a window onto disease mechanism, potentially generating therapeutic targets for disease. In particular, biomarkers enable investigation of the premotor period of PD before typical symptoms are manifest, but while degeneration has already begun. Given the multiple genetic causes for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset and the clear heterogeneity of clinical symptoms in PD onset and clinical progression, it is likely many biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms will be necessary to fully map PD risk and progression. Biomarkers are also critical in new drug development for PD, both in early validation studies to assess drug dosing and to determine drug penetrance into the brain, and in later efficacy studies to complement PD clinical outcomes. During the past two decades, much progress has been made in identifying and assessing PD biomarkers, but as yet, no fully validated biomarker for PD is currently available. Nonetheless, there is increasing evidence that molecular genetics, focused <i>‐omic</i> (proteomic, metabolomic, and transcriptomic) assessment of blood and cerebrospinal fluid, and advanced in vivo brain imaging will provide critical clues to assist in the diagnosis and medical management of PD patients. Ann Neurol 2008;64 (suppl):S111–S121</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflicts of interest: This article is part of a supplement sponsored by Boehringer Ingelheim (BI). K.M. has served as a consultant for BI, Pfizer, Novartis, GE Health, Alseres, Merck Serono, Lilly, Bayer Schering Pharma, Elan, and has equity interest in Molecular NeuroImaging, LLC. D.J. is a consultant for BI, Genzyme and Teva. D.J. is an employee of Molecular NeuroImaging, LLC. G.T. has no financial interests to disclose. J.P.S. has served as a consultant for BI, Avid Radiopharmaceuticals, Bayer Schering Healthcare, Pfizer, Takeda Pharmaceuticals, Lilly, GE Healthcare, Alseres, Novartis, Eisai, and has equity interest in Molecular Neuroimaging, LLC.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Biomarkers for Parkison's disease: Tools to assess Parkinson's disease onset and progression</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Biomarkers for PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Biomarkers for Parkison's disease: Tools to assess Parkinson's disease onset and progression</title></titleInfo><name type="personal"><namePart type="given">Kenneth</namePart><namePart type="family">Marek</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation><description>Correspondence: Institute for Neurodegenerative Disorders, 60 Temple Street, New Haven, CT 06510</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Danna</namePart><namePart type="family">Jennings</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gilles</namePart><namePart type="family">Tamagnan</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John</namePart><namePart type="family">Seibyl</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Institute for Neurodegenerative Disorders, New Haven, CT</affiliation><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">2008-12</dateIssued><dateCaptured encoding="w3cdtf">2008-03-19</dateCaptured><dateValid encoding="w3cdtf">2008-11-07</dateValid><copyrightDate encoding="w3cdtf">2008</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">1</extent><extent unit="tables">2</extent><extent unit="references">128</extent><extent unit="words">8360</extent></physicalDescription><abstract lang="en">Reliable and well‐validated biomarkers for PD to identify individuals “at risk” before motor symptoms, accurately diagnose individuals at the threshold of clinical PD, and monitor PD progression throughout its course would dramatically accelerate research into both PD cause and therapeutics. Biomarkers offer the potential to provide a window onto disease mechanism, potentially generating therapeutic targets for disease. In particular, biomarkers enable investigation of the premotor period of PD before typical symptoms are manifest, but while degeneration has already begun. Given the multiple genetic causes for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset and the clear heterogeneity of clinical symptoms in PD onset and clinical progression, it is likely many biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms will be necessary to fully map PD risk and progression. Biomarkers are also critical in new drug development for PD, both in early validation studies to assess drug dosing and to determine drug penetrance into the brain, and in later efficacy studies to complement PD clinical outcomes. During the past two decades, much progress has been made in identifying and assessing PD biomarkers, but as yet, no fully validated biomarker for PD is currently available. Nonetheless, there is increasing evidence that molecular genetics, focused ‐omic (proteomic, metabolomic, and transcriptomic) assessment of blood and cerebrospinal fluid, and advanced in vivo brain imaging will provide critical clues to assist in the diagnosis and medical management of PD patients. Ann Neurol 2008;64 (suppl):S111–S121</abstract><note type="content">*Potential conflicts of interest: This article is part of a supplement sponsored by Boehringer Ingelheim (BI). K.M. has served as a consultant for BI, Pfizer, Novartis, GE Health, Alseres, Merck Serono, Lilly, Bayer Schering Pharma, Elan, and has equity interest in Molecular NeuroImaging, LLC. D.J. is a consultant for BI, Genzyme and Teva. D.J. is an employee of Molecular NeuroImaging, LLC. G.T. has no financial interests to disclose. J.P.S. has served as a consultant for BI, Avid Radiopharmaceuticals, Bayer Schering Healthcare, Pfizer, Takeda Pharmaceuticals, Lilly, GE Healthcare, Alseres, Novartis, Eisai, and has equity interest in Molecular Neuroimaging, LLC.</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.</note><subject><genre>article category</genre><topic>Future Issues</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>64</number></detail><detail type="issue"><caption>no.</caption><number>S2</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>2</number></detail><extent unit="pages"><start>S111</start><end>S121</end><total>11</total></extent></part></relatedItem><identifier type="istex">0EEFB35A16B0C4B53498468A4125CA19E9BC5EC2</identifier><identifier type="DOI">10.1002/ana.21602</identifier><identifier type="ArticleID">ANA21602</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 American Neurological Association</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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