Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression
Identifieur interne : 000105 ( Main/Corpus ); précédent : 000104; suivant : 000106Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression
Auteurs : Min Shi ; Joshua Bradner ; Aneeka M. Hancock ; Kathryn A. Chung ; Joseph F. Quinn ; Elaine R. Peskind ; Douglas Galasko ; Joseph Jankovic ; Cyrus P. Zabetian ; Hojoong M. Kim ; James B. Leverenz ; Thomas J. Montine ; Carmen Ginghina ; Un Jung Kang ; Kevin C. Cain ; Yu Wang ; Jan Aasly ; David Goldstein ; Jing ZhangSource :
- Annals of Neurology [ 0364-5134 ] ; 2011-03.
Abstract
Objective:: There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. We and others have demonstrated that a decrease in DJ‐1 and/or α‐synuclein in the cerebrospinal fluid (CSF) is a potential index for Parkinson disease diagnosis, but not for PD severity. Methods:: Using highly sensitive and quantitative Luminex assays, we measured total tau, phosphorylated tau, amyloid beta peptide 1–42 (Aβ1–42), Flt3 ligand, and fractalkine levels in CSF in a large cohort of PD patients at different stages as well as healthy and diseased controls. The utility of these 5 markers was evaluated for disease diagnosis and severity/progression correlation alone, as well as in combination with DJ‐1 and α‐synuclein. The major results were further validated in an independent cohort of cross‐sectional PD patients as well as in PD cases with CSF samples collected longitudinally. Results:: The results demonstrated that combinations of these biomarkers could differentiate PD patients not only from normal controls but also from patients with Alzheimer disease (AD) and multiple system atrophy. Particularly, with CSF Flt3 ligand, PD could be clearly differentiated from multiple system atrophy, a disease that overlaps with PD clinically, with excellent sensitivity (99%) and specificity (95%). In addition, we identified CSF fractalkine/Aβ1–42 that positively correlated with PD severity in cross‐sectional samples as well as with PD progression in longitudinal samples. Interpretation:: We have demonstrated that this panel of 7 CSF proteins could aid in Parkinson disease diagnosis, differential diagnosis, and correlation with disease severity and progression. ANN NEUROL 2010
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DOI: 10.1002/ana.22311
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Cain</name><affiliation><mods:affiliation>Department of Biostatistics, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Wang, Yu" sort="Wang, Yu" uniqKey="Wang Y" first="Yu" last="Wang">Yu Wang</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China</mods:affiliation></affiliation></author><author><name sortKey="Aasly, Jan" sort="Aasly, Jan" uniqKey="Aasly J" first="Jan" last="Aasly">Jan Aasly</name><affiliation><mods:affiliation>Department of Neurology, St. Olavs Hospital, Trondheim, Norway</mods:affiliation></affiliation></author><author><name sortKey="Goldstein, David" sort="Goldstein, David" uniqKey="Goldstein D" first="David" last="Goldstein">David Goldstein</name><affiliation><mods:affiliation>Clinical Neurocardiology Section, Community Networks Program (CNP), Division of Intramural Research (DIR), National Institute for Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD</mods:affiliation></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/ana.22311</idno><idno type="url">https://api.istex.fr/document/9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000105</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression</title><author><name sortKey="Shi, Min" sort="Shi, Min" uniqKey="Shi M" first="Min" last="Shi">Min Shi</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Bradner, Joshua" sort="Bradner, Joshua" uniqKey="Bradner J" first="Joshua" last="Bradner">Joshua Bradner</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Hancock, Aneeka M" sort="Hancock, Aneeka M" uniqKey="Hancock A" first="Aneeka M." last="Hancock">Aneeka M. Hancock</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Chung, Kathryn A" sort="Chung, Kathryn A" uniqKey="Chung K" first="Kathryn A." last="Chung">Kathryn A. Chung</name><affiliation><mods:affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</mods:affiliation></affiliation></author><author><name sortKey="Quinn, Joseph F" sort="Quinn, Joseph F" uniqKey="Quinn J" first="Joseph F." last="Quinn">Joseph F. Quinn</name><affiliation><mods:affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</mods:affiliation></affiliation></author><author><name sortKey="Peskind, Elaine R" sort="Peskind, Elaine R" uniqKey="Peskind E" first="Elaine R." last="Peskind">Elaine R. Peskind</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Galasko, Douglas" sort="Galasko, Douglas" uniqKey="Galasko D" first="Douglas" last="Galasko">Douglas Galasko</name><affiliation><mods:affiliation>Department of Neurosciences, University of California at San Diego, San Diego, CA</mods:affiliation></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name><affiliation><mods:affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX</mods:affiliation></affiliation></author><author><name sortKey="Zabetian, Cyrus P" sort="Zabetian, Cyrus P" uniqKey="Zabetian C" first="Cyrus P." last="Zabetian">Cyrus P. Zabetian</name><affiliation><mods:affiliation>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Kim, Hojoong M" sort="Kim, Hojoong M" uniqKey="Kim H" first="Hojoong M." last="Kim">Hojoong M. Kim</name><affiliation><mods:affiliation>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Leverenz, James B" sort="Leverenz, James B" uniqKey="Leverenz J" first="James B." last="Leverenz">James B. Leverenz</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Montine, Thomas J" sort="Montine, Thomas J" uniqKey="Montine T" first="Thomas J." last="Montine">Thomas J. Montine</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Ginghina, Carmen" sort="Ginghina, Carmen" uniqKey="Ginghina C" first="Carmen" last="Ginghina">Carmen Ginghina</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Kang, Un Jung" sort="Kang, Un Jung" uniqKey="Kang U" first="Un Jung" last="Kang">Un Jung Kang</name><affiliation><mods:affiliation>Department of Neurology, University of Chicago, Chicago, IL</mods:affiliation></affiliation></author><author><name sortKey="Cain, Kevin C" sort="Cain, Kevin C" uniqKey="Cain K" first="Kevin C." last="Cain">Kevin C. Cain</name><affiliation><mods:affiliation>Department of Biostatistics, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author><author><name sortKey="Wang, Yu" sort="Wang, Yu" uniqKey="Wang Y" first="Yu" last="Wang">Yu Wang</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China</mods:affiliation></affiliation></author><author><name sortKey="Aasly, Jan" sort="Aasly, Jan" uniqKey="Aasly J" first="Jan" last="Aasly">Jan Aasly</name><affiliation><mods:affiliation>Department of Neurology, St. Olavs Hospital, Trondheim, Norway</mods:affiliation></affiliation></author><author><name sortKey="Goldstein, David" sort="Goldstein, David" uniqKey="Goldstein D" first="David" last="Goldstein">David Goldstein</name><affiliation><mods:affiliation>Clinical Neurocardiology Section, Community Networks Program (CNP), Division of Intramural Research (DIR), National Institute for Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD</mods:affiliation></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-03">2011-03</date><biblScope unit="volume">69</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="570">570</biblScope><biblScope unit="page" to="580">580</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524</idno><idno type="DOI">10.1002/ana.22311</idno><idno type="ArticleID">ANA22311</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective:: There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. We and others have demonstrated that a decrease in DJ‐1 and/or α‐synuclein in the cerebrospinal fluid (CSF) is a potential index for Parkinson disease diagnosis, but not for PD severity. Methods:: Using highly sensitive and quantitative Luminex assays, we measured total tau, phosphorylated tau, amyloid beta peptide 1–42 (Aβ1–42), Flt3 ligand, and fractalkine levels in CSF in a large cohort of PD patients at different stages as well as healthy and diseased controls. The utility of these 5 markers was evaluated for disease diagnosis and severity/progression correlation alone, as well as in combination with DJ‐1 and α‐synuclein. The major results were further validated in an independent cohort of cross‐sectional PD patients as well as in PD cases with CSF samples collected longitudinally. Results:: The results demonstrated that combinations of these biomarkers could differentiate PD patients not only from normal controls but also from patients with Alzheimer disease (AD) and multiple system atrophy. Particularly, with CSF Flt3 ligand, PD could be clearly differentiated from multiple system atrophy, a disease that overlaps with PD clinically, with excellent sensitivity (99%) and specificity (95%). In addition, we identified CSF fractalkine/Aβ1–42 that positively correlated with PD severity in cross‐sectional samples as well as with PD progression in longitudinal samples. Interpretation:: We have demonstrated that this panel of 7 CSF proteins could aid in Parkinson disease diagnosis, differential diagnosis, and correlation with disease severity and progression. ANN NEUROL 2010</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Min Shi PhD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Joshua Bradner MS</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Aneeka M. Hancock BS</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Kathryn A. Chung MD</name><affiliations><json:string>Department of Neurology, Oregon Health and Science University, Portland, OR</json:string></affiliations></json:item><json:item><name>Joseph F. Quinn MD</name><affiliations><json:string>Department of Neurology, Oregon Health and Science University, Portland, OR</json:string></affiliations></json:item><json:item><name>Elaine R. Peskind MD</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</json:string><json:string>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</json:string></affiliations></json:item><json:item><name>Douglas Galasko MD</name><affiliations><json:string>Department of Neurosciences, University of California at San Diego, San Diego, CA</json:string></affiliations></json:item><json:item><name>Joseph Jankovic MD</name><affiliations><json:string>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX</json:string></affiliations></json:item><json:item><name>Cyrus P. Zabetian MD</name><affiliations><json:string>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Hojoong M. Kim MD</name><affiliations><json:string>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>James B. Leverenz MD</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</json:string><json:string>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Thomas J. Montine MD, PhD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Carmen Ginghina MD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Un Jung Kang MD</name><affiliations><json:string>Department of Neurology, University of Chicago, Chicago, IL</json:string></affiliations></json:item><json:item><name>Kevin C. Cain PhD</name><affiliations><json:string>Department of Biostatistics, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item><json:item><name>Yu Wang MD, PhD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, WA</json:string><json:string>Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China</json:string></affiliations></json:item><json:item><name>Jan Aasly MD</name><affiliations><json:string>Department of Neurology, St. Olavs Hospital, Trondheim, Norway</json:string></affiliations></json:item><json:item><name>David Goldstein MD, PhD</name><affiliations><json:string>Clinical Neurocardiology Section, Community Networks Program (CNP), Division of Intramural Research (DIR), National Institute for Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD</json:string></affiliations></json:item><json:item><name>Jing Zhang MD, PhD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, WA</json:string></affiliations></json:item></author><articleId><json:string>ANA22311</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objective:: There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. We and others have demonstrated that a decrease in DJ‐1 and/or α‐synuclein in the cerebrospinal fluid (CSF) is a potential index for Parkinson disease diagnosis, but not for PD severity. Methods:: Using highly sensitive and quantitative Luminex assays, we measured total tau, phosphorylated tau, amyloid beta peptide 1–42 (Aβ1–42), Flt3 ligand, and fractalkine levels in CSF in a large cohort of PD patients at different stages as well as healthy and diseased controls. The utility of these 5 markers was evaluated for disease diagnosis and severity/progression correlation alone, as well as in combination with DJ‐1 and α‐synuclein. The major results were further validated in an independent cohort of cross‐sectional PD patients as well as in PD cases with CSF samples collected longitudinally. Results:: The results demonstrated that combinations of these biomarkers could differentiate PD patients not only from normal controls but also from patients with Alzheimer disease (AD) and multiple system atrophy. Particularly, with CSF Flt3 ligand, PD could be clearly differentiated from multiple system atrophy, a disease that overlaps with PD clinically, with excellent sensitivity (99%) and specificity (95%). In addition, we identified CSF fractalkine/Aβ1–42 that positively correlated with PD severity in cross‐sectional samples as well as with PD progression in longitudinal samples. Interpretation:: We have demonstrated that this panel of 7 CSF proteins could aid in Parkinson disease diagnosis, differential diagnosis, and correlation with disease severity and progression. ANN NEUROL 2010</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 801 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1778</abstractCharCount><pdfWordCount>6827</pdfWordCount><pdfCharCount>43478</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>256</abstractWordCount></qualityIndicators><title>Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression</title><genre><json:string>article</json:string></genre><host><volume>69</volume><publisherId><json:string>ANA</json:string></publisherId><pages><total>11</total><last>580</last><first>570</first></pages><issn><json:string>0364-5134</json:string></issn><issue>3</issue><subject><json:item><value>Original Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8249</json:string></eissn><title>Annals of Neurology</title><doi><json:string>10.1002/(ISSN)1531-8249</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/ana.22311</json:string></doi><id>9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note>Supplementary Figures and TablesSupplementary Methods</note><note type="content">*This manuscript first appeared online on 28 October 2010 as an Accepted Article on onlinelibrary.wiley.com.</note><note>NIH - No. ES004696;</note><note>NIEHS - No. NS057567; No. NS060252; No. NS062684;</note><note>NINDS - No. AG025327; No. AG033398; No. AG005136; No. AG008017;</note><note>NIA - No. UL1RR025014;</note><note>NCRR</note><note>Dana Foundation</note><note>Parkinson's Disease Foundation</note><note>Michael J. Fox Foundation</note><note>Friends of Alzheimer's Research</note><note>Alzheimer's Association of Western and Central Washington</note><note>Department of Veterans Affairs</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression</title><author><persName><forename type="first">Min</forename><surname>Shi</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Joshua</forename><surname>Bradner</surname></persName><roleName type="degree">MS</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Aneeka M.</forename><surname>Hancock</surname></persName><roleName type="degree">BS</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Kathryn A.</forename><surname>Chung</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</affiliation></author><author><persName><forename type="first">Joseph F.</forename><surname>Quinn</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</affiliation></author><author><persName><forename type="first">Elaine R.</forename><surname>Peskind</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation></author><author><persName><forename type="first">Douglas</forename><surname>Galasko</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurosciences, University of California at San Diego, San Diego, CA</affiliation></author><author><persName><forename type="first">Joseph</forename><surname>Jankovic</surname></persName><roleName type="degree">MD</roleName><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX</affiliation></author><author><persName><forename type="first">Cyrus P.</forename><surname>Zabetian</surname></persName><roleName type="degree">MD</roleName><affiliation>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Hojoong M.</forename><surname>Kim</surname></persName><roleName type="degree">MD</roleName><affiliation>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">James B.</forename><surname>Leverenz</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Thomas J.</forename><surname>Montine</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Carmen</forename><surname>Ginghina</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Un Jung</forename><surname>Kang</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, University of Chicago, Chicago, IL</affiliation></author><author><persName><forename type="first">Kevin C.</forename><surname>Cain</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Biostatistics, University of Washington School of Medicine, Seattle, WA</affiliation></author><author><persName><forename type="first">Yu</forename><surname>Wang</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China</affiliation></author><author><persName><forename type="first">Jan</forename><surname>Aasly</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, St. Olavs Hospital, Trondheim, Norway</affiliation></author><author><persName><forename type="first">David</forename><surname>Goldstein</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Clinical Neurocardiology Section, Community Networks Program (CNP), Division of Intramural Research (DIR), National Institute for Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD</affiliation></author><author><persName><forename type="first">Jing</forename><surname>Zhang</surname></persName><roleName type="degree">MD, PhD</roleName><note type="correspondence"><p>Correspondence: Department of Pathology, University of Washington School of Medicine, HMC Box 359635, 325 9th Ave, Seattle, WA 98104</p></note><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</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="2011-03"></date><biblScope unit="volume">69</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="570">570</biblScope><biblScope unit="page" to="580">580</biblScope></imprint></monogr><idno type="istex">9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524</idno><idno type="DOI">10.1002/ana.22311</idno><idno type="ArticleID">ANA22311</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objective:: There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. We and others have demonstrated that a decrease in DJ‐1 and/or α‐synuclein in the cerebrospinal fluid (CSF) is a potential index for Parkinson disease diagnosis, but not for PD severity. Methods:: Using highly sensitive and quantitative Luminex assays, we measured total tau, phosphorylated tau, amyloid beta peptide 1–42 (Aβ1–42), Flt3 ligand, and fractalkine levels in CSF in a large cohort of PD patients at different stages as well as healthy and diseased controls. The utility of these 5 markers was evaluated for disease diagnosis and severity/progression correlation alone, as well as in combination with DJ‐1 and α‐synuclein. The major results were further validated in an independent cohort of cross‐sectional PD patients as well as in PD cases with CSF samples collected longitudinally. Results:: The results demonstrated that combinations of these biomarkers could differentiate PD patients not only from normal controls but also from patients with Alzheimer disease (AD) and multiple system atrophy. Particularly, with CSF Flt3 ligand, PD could be clearly differentiated from multiple system atrophy, a disease that overlaps with PD clinically, with excellent sensitivity (99%) and specificity (95%). In addition, we identified CSF fractalkine/Aβ1–42 that positively correlated with PD severity in cross‐sectional samples as well as with PD progression in longitudinal samples. Interpretation:: We have demonstrated that this panel of 7 CSF proteins could aid in Parkinson disease diagnosis, differential diagnosis, and correlation with disease severity and progression. ANN NEUROL 2010</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-07-01">Received</change><change when="2010-10-15">Registration</change><change when="2011-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524/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 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College, Huazhong University of Science and Technology, Wuhan, China</unparsedAffiliation></affiliation><affiliation xml:id="af12" countryCode="NO" type="organization"><unparsedAffiliation>Department of Neurology, St. Olavs Hospital, Trondheim, Norway</unparsedAffiliation></affiliation><affiliation xml:id="af13" countryCode="US" type="organization"><unparsedAffiliation>Clinical Neurocardiology Section, Community Networks Program (CNP), Division of Intramural Research (DIR), National Institute for Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD</unparsedAffiliation></affiliation></affiliationGroup><fundingInfo><fundingAgency>NIH</fundingAgency><fundingNumber>ES004696</fundingNumber></fundingInfo><fundingInfo><fundingAgency>NIEHS</fundingAgency><fundingNumber>NS057567</fundingNumber><fundingNumber>NS060252</fundingNumber><fundingNumber>NS062684</fundingNumber></fundingInfo><fundingInfo><fundingAgency>NINDS</fundingAgency><fundingNumber>AG025327</fundingNumber><fundingNumber>AG033398</fundingNumber><fundingNumber>AG005136</fundingNumber><fundingNumber>AG008017</fundingNumber></fundingInfo><fundingInfo><fundingAgency>NIA</fundingAgency><fundingNumber>UL1RR025014</fundingNumber></fundingInfo><fundingInfo><fundingAgency>NCRR</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Dana Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Parkinson's Disease Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Michael J. Fox Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Friends of Alzheimer's Research</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Alzheimer's Association of Western and Central Washington</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Department of Veterans Affairs</fundingAgency></fundingInfo><supportingInformation><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana22311:ANA_22311_Suppl_Figures_and_Tables"></mediaResource><caption>Supplementary Figures and Tables</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:03645134:media:ana22311:ANA_22311_Suppl_Methods"></mediaResource><caption>Supplementary Methods</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><section xml:id="abs1-1"><title type="main">Objective:</title><p>There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. We and others have demonstrated that a decrease in DJ‐1 and/or α‐synuclein in the cerebrospinal fluid (CSF) is a potential index for Parkinson disease diagnosis, but not for PD severity.</p></section><section xml:id="abs1-2"><title type="main">Methods:</title><p>Using highly sensitive and quantitative Luminex assays, we measured total tau, phosphorylated tau, amyloid beta peptide 1–42 (Aβ<sub>1–42</sub>), Flt3 ligand, and fractalkine levels in CSF in a large cohort of PD patients at different stages as well as healthy and diseased controls. The utility of these 5 markers was evaluated for disease diagnosis and severity/progression correlation alone, as well as in combination with DJ‐1 and α‐synuclein. The major results were further validated in an independent cohort of cross‐sectional PD patients as well as in PD cases with CSF samples collected longitudinally.</p></section><section xml:id="abs1-3"><title type="main">Results:</title><p>The results demonstrated that combinations of these biomarkers could differentiate PD patients not only from normal controls but also from patients with Alzheimer disease (AD) and multiple system atrophy. Particularly, with CSF Flt3 ligand, PD could be clearly differentiated from multiple system atrophy, a disease that overlaps with PD clinically, with excellent sensitivity (99%) and specificity (95%). In addition, we identified CSF fractalkine/Aβ<sub>1–42</sub> that positively correlated with PD severity in cross‐sectional samples as well as with PD progression in longitudinal samples.</p></section><section xml:id="abs1-4"><title type="main">Interpretation:</title><p>We have demonstrated that this panel of 7 CSF proteins could aid in Parkinson disease diagnosis, differential diagnosis, and correlation with disease severity and progression. ANN NEUROL 2010</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>This manuscript first appeared online on 28 October 2010 as an Accepted Article on onlinelibrary.wiley.com.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CSF Biomarkers for PD Diagnosis and Progression</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cerebrospinal fluid biomarkers for Parkinson disease diagnosis and progression</title></titleInfo><name type="personal"><namePart type="given">Min</namePart><namePart type="family">Shi</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joshua</namePart><namePart type="family">Bradner</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Aneeka M.</namePart><namePart type="family">Hancock</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kathryn A.</namePart><namePart type="family">Chung</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph F.</namePart><namePart type="family">Quinn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Oregon Health and Science University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elaine R.</namePart><namePart type="family">Peskind</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Douglas</namePart><namePart type="family">Galasko</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosciences, University of California at San Diego, San Diego, CA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Jankovic</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cyrus P.</namePart><namePart type="family">Zabetian</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hojoong M.</namePart><namePart type="family">Kim</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Geriatric Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">James B.</namePart><namePart type="family">Leverenz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Mental Illness Research, Education, and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas J.</namePart><namePart type="family">Montine</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carmen</namePart><namePart type="family">Ginghina</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Un Jung</namePart><namePart type="family">Kang</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University of Chicago, Chicago, IL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kevin C.</namePart><namePart type="family">Cain</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biostatistics, University of Washington School of Medicine, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yu</namePart><namePart type="family">Wang</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><affiliation>Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan</namePart><namePart type="family">Aasly</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, St. Olavs Hospital, Trondheim, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David</namePart><namePart type="family">Goldstein</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Clinical Neurocardiology Section, Community Networks Program (CNP), Division of Intramural Research (DIR), National Institute for Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH), Bethesda, MD</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jing</namePart><namePart type="family">Zhang</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, WA</affiliation><description>Correspondence: Department of Pathology, University of Washington School of Medicine, HMC Box 359635, 325 9th Ave, Seattle, WA 98104</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">2011-03</dateIssued><dateCaptured encoding="w3cdtf">2010-07-01</dateCaptured><dateValid encoding="w3cdtf">2010-10-15</dateValid><copyrightDate encoding="w3cdtf">2011</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">52</extent><extent unit="words">7443</extent></physicalDescription><abstract lang="en">Objective:: There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. We and others have demonstrated that a decrease in DJ‐1 and/or α‐synuclein in the cerebrospinal fluid (CSF) is a potential index for Parkinson disease diagnosis, but not for PD severity. Methods:: Using highly sensitive and quantitative Luminex assays, we measured total tau, phosphorylated tau, amyloid beta peptide 1–42 (Aβ1–42), Flt3 ligand, and fractalkine levels in CSF in a large cohort of PD patients at different stages as well as healthy and diseased controls. The utility of these 5 markers was evaluated for disease diagnosis and severity/progression correlation alone, as well as in combination with DJ‐1 and α‐synuclein. The major results were further validated in an independent cohort of cross‐sectional PD patients as well as in PD cases with CSF samples collected longitudinally. Results:: The results demonstrated that combinations of these biomarkers could differentiate PD patients not only from normal controls but also from patients with Alzheimer disease (AD) and multiple system atrophy. Particularly, with CSF Flt3 ligand, PD could be clearly differentiated from multiple system atrophy, a disease that overlaps with PD clinically, with excellent sensitivity (99%) and specificity (95%). In addition, we identified CSF fractalkine/Aβ1–42 that positively correlated with PD severity in cross‐sectional samples as well as with PD progression in longitudinal samples. Interpretation:: We have demonstrated that this panel of 7 CSF proteins could aid in Parkinson disease diagnosis, differential diagnosis, and correlation with disease severity and progression. ANN NEUROL 2010</abstract><note type="additional physical form">Supplementary Figures and TablesSupplementary Methods</note><note type="content">*This manuscript first appeared online on 28 October 2010 as an Accepted Article on onlinelibrary.wiley.com.</note><note type="funding">NIH - No. ES004696; </note><note type="funding">NIEHS - No. NS057567; No. NS060252; No. NS062684; </note><note type="funding">NINDS - No. AG025327; No. AG033398; No. AG005136; No. AG008017; </note><note type="funding">NIA - No. UL1RR025014; </note><note type="funding">NCRR</note><note type="funding">Dana Foundation</note><note type="funding">Parkinson's Disease Foundation</note><note type="funding">Michael J. Fox Foundation</note><note type="funding">Friends of Alzheimer's Research</note><note type="funding">Alzheimer's Association of Western and Central Washington</note><note type="funding">Department of Veterans Affairs</note><relatedItem type="host"><titleInfo><title>Annals of Neurology</title></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Article</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>2011</date><detail type="volume"><caption>vol.</caption><number>69</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>570</start><end>580</end><total>11</total></extent></part></relatedItem><identifier type="istex">9B5D1E4D5793173EFBDFC7B257C2BFFEC943F524</identifier><identifier type="DOI">10.1002/ana.22311</identifier><identifier type="ArticleID">ANA22311</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 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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