Association of cerebrospinal fluid β-amyloid 1-42, T-tau, P-tau181, and α-synuclein levels with clinical features of drug-naive patients with early Parkinson disease.
Identifieur interne : 000042 ( PubMed/Corpus ); précédent : 000041; suivant : 000043Association of cerebrospinal fluid β-amyloid 1-42, T-tau, P-tau181, and α-synuclein levels with clinical features of drug-naive patients with early Parkinson disease.
Auteurs : Ju Kang ; David. Irwin ; Alice. Chen ; Andrew Siderowf ; Chelsea Caspell ; Christopher. Coffey ; Teresa Walig ; Peggy Taylor ; Sarah Pan ; Mark Frasier ; Kenneth Marek ; Karl Kieburtz ; Danna Jennings ; Tanya Simuni ; Caroline. Tanner ; Andrew Singleton ; Arthur. Toga ; Sohini Chowdhury ; Brit Mollenhauer ; John. Trojanowski ; Leslie. ShawSource :
- JAMA neurology ; 2013.
English descriptors
- KwdEn :
- Amyloid beta-Peptides (cerebrospinal fluid), Case-Control Studies, Cohort Studies, Female, Humans, Male, Memory (physiology), Middle Aged, Movement (physiology), Neuropsychological Tests, Parkinson Disease (cerebrospinal fluid), Parkinson Disease (physiopathology), Peptide Fragments (cerebrospinal fluid), Phosphorylation, Regression Analysis, Severity of Illness Index, Statistics as Topic, Threonine (metabolism), Verbal Learning (physiology), alpha-Synuclein (cerebrospinal fluid), tau Proteins (cerebrospinal fluid).
- MESH :
- chemical , cerebrospinal fluid : Amyloid beta-Peptides, Peptide Fragments, alpha-Synuclein, tau Proteins.
- cerebrospinal fluid : Parkinson Disease.
- chemical , metabolism : Threonine.
- physiology : Memory, Movement, Verbal Learning.
- physiopathology : Parkinson Disease.
- Case-Control Studies, Cohort Studies, Female, Humans, Male, Middle Aged, Neuropsychological Tests, Phosphorylation, Regression Analysis, Severity of Illness Index, Statistics as Topic.
Abstract
We observed a significant correlation between cerebrospinal fluid (CSF) levels of tau proteins and α-synuclein, but not β-amyloid 1-42 (Aβ1-42), and lower concentration of CSF biomarkers, as compared with healthy controls, in a cohort of entirely untreated patients with Parkinson disease (PD) at the earliest stage of the disease studied so far.
DOI: 10.1001/jamaneurol.2013.3861
PubMed: 23979011
Links to Exploration step
pubmed:23979011Le document en format XML
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Chen</name></author><author><name sortKey="Siderowf, Andrew" sort="Siderowf, Andrew" uniqKey="Siderowf A" first="Andrew" last="Siderowf">Andrew Siderowf</name></author><author><name sortKey="Caspell, Chelsea" sort="Caspell, Chelsea" uniqKey="Caspell C" first="Chelsea" last="Caspell">Chelsea Caspell</name></author><author><name sortKey="Coffey, Christopher S" sort="Coffey, Christopher S" uniqKey="Coffey C" first="Christopher" last="Coffey">Christopher. Coffey</name></author><author><name sortKey="Walig Rska, Teresa" sort="Walig Rska, Teresa" uniqKey="Walig Rska T" first="Teresa" last="Walig">Teresa Walig</name></author><author><name sortKey="Taylor, Peggy" sort="Taylor, Peggy" uniqKey="Taylor P" first="Peggy" last="Taylor">Peggy Taylor</name></author><author><name sortKey="Pan, Sarah" sort="Pan, Sarah" uniqKey="Pan S" first="Sarah" last="Pan">Sarah Pan</name></author><author><name sortKey="Frasier, Mark" sort="Frasier, Mark" uniqKey="Frasier M" first="Mark" last="Frasier">Mark Frasier</name></author><author><name sortKey="Marek, Kenneth" sort="Marek, Kenneth" uniqKey="Marek K" first="Kenneth" last="Marek">Kenneth Marek</name></author><author><name sortKey="Kieburtz, Karl" sort="Kieburtz, Karl" uniqKey="Kieburtz K" first="Karl" last="Kieburtz">Karl Kieburtz</name></author><author><name sortKey="Jennings, Danna" sort="Jennings, Danna" uniqKey="Jennings D" first="Danna" last="Jennings">Danna Jennings</name></author><author><name sortKey="Simuni, Tanya" sort="Simuni, Tanya" uniqKey="Simuni T" first="Tanya" last="Simuni">Tanya Simuni</name></author><author><name sortKey="Tanner, Caroline M" sort="Tanner, Caroline M" uniqKey="Tanner C" first="Caroline" last="Tanner">Caroline. 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Shaw</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="doi">10.1001/jamaneurol.2013.3861</idno><idno type="RBID">pubmed:23979011</idno><idno type="pmid">23979011</idno><idno type="wicri:Area/PubMed/Corpus">000042</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Association of cerebrospinal fluid β-amyloid 1-42, T-tau, P-tau181, and α-synuclein levels with clinical features of drug-naive patients with early Parkinson disease.</title><author><name sortKey="Kang, Ju Hee" sort="Kang, Ju Hee" uniqKey="Kang J" first="Ju" last="Kang">Ju Kang</name></author><author><name sortKey="Irwin, David J" sort="Irwin, David J" uniqKey="Irwin D" first="David" last="Irwin">David. Irwin</name></author><author><name sortKey="Chen Plotkin, Alice S" sort="Chen Plotkin, Alice S" uniqKey="Chen Plotkin A" first="Alice" last="Chen">Alice. Chen</name></author><author><name sortKey="Siderowf, Andrew" sort="Siderowf, Andrew" uniqKey="Siderowf A" first="Andrew" last="Siderowf">Andrew Siderowf</name></author><author><name sortKey="Caspell, Chelsea" sort="Caspell, Chelsea" uniqKey="Caspell C" first="Chelsea" last="Caspell">Chelsea Caspell</name></author><author><name sortKey="Coffey, Christopher S" sort="Coffey, Christopher S" uniqKey="Coffey C" first="Christopher" last="Coffey">Christopher. Coffey</name></author><author><name sortKey="Walig Rska, Teresa" sort="Walig Rska, Teresa" uniqKey="Walig Rska T" first="Teresa" last="Walig">Teresa Walig</name></author><author><name sortKey="Taylor, Peggy" sort="Taylor, Peggy" uniqKey="Taylor P" first="Peggy" last="Taylor">Peggy Taylor</name></author><author><name sortKey="Pan, Sarah" sort="Pan, Sarah" uniqKey="Pan S" first="Sarah" last="Pan">Sarah Pan</name></author><author><name sortKey="Frasier, Mark" sort="Frasier, Mark" uniqKey="Frasier M" first="Mark" last="Frasier">Mark Frasier</name></author><author><name sortKey="Marek, Kenneth" sort="Marek, Kenneth" uniqKey="Marek K" first="Kenneth" last="Marek">Kenneth Marek</name></author><author><name sortKey="Kieburtz, Karl" sort="Kieburtz, Karl" uniqKey="Kieburtz K" first="Karl" last="Kieburtz">Karl Kieburtz</name></author><author><name sortKey="Jennings, Danna" sort="Jennings, Danna" uniqKey="Jennings D" first="Danna" last="Jennings">Danna Jennings</name></author><author><name sortKey="Simuni, Tanya" sort="Simuni, Tanya" uniqKey="Simuni T" first="Tanya" last="Simuni">Tanya Simuni</name></author><author><name sortKey="Tanner, Caroline M" sort="Tanner, Caroline M" uniqKey="Tanner C" first="Caroline" last="Tanner">Caroline. Tanner</name></author><author><name sortKey="Singleton, Andrew" sort="Singleton, Andrew" uniqKey="Singleton A" first="Andrew" last="Singleton">Andrew Singleton</name></author><author><name sortKey="Toga, Arthur W" sort="Toga, Arthur W" uniqKey="Toga A" first="Arthur" last="Toga">Arthur. Toga</name></author><author><name sortKey="Chowdhury, Sohini" sort="Chowdhury, Sohini" uniqKey="Chowdhury S" first="Sohini" last="Chowdhury">Sohini Chowdhury</name></author><author><name sortKey="Mollenhauer, Brit" sort="Mollenhauer, Brit" uniqKey="Mollenhauer B" first="Brit" last="Mollenhauer">Brit Mollenhauer</name></author><author><name sortKey="Trojanowski, John Q" sort="Trojanowski, John Q" uniqKey="Trojanowski J" first="John" last="Trojanowski">John. Trojanowski</name></author><author><name sortKey="Shaw, Leslie M" sort="Shaw, Leslie M" uniqKey="Shaw L" first="Leslie" last="Shaw">Leslie. Shaw</name></author></analytic><series><title level="j">JAMA neurology</title><idno type="e-ISSN">2168-6157</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amyloid beta-Peptides (cerebrospinal fluid)</term><term>Case-Control Studies</term><term>Cohort Studies</term><term>Female</term><term>Humans</term><term>Male</term><term>Memory (physiology)</term><term>Middle Aged</term><term>Movement (physiology)</term><term>Neuropsychological Tests</term><term>Parkinson Disease (cerebrospinal fluid)</term><term>Parkinson Disease (physiopathology)</term><term>Peptide Fragments (cerebrospinal fluid)</term><term>Phosphorylation</term><term>Regression Analysis</term><term>Severity of Illness Index</term><term>Statistics as Topic</term><term>Threonine (metabolism)</term><term>Verbal Learning (physiology)</term><term>alpha-Synuclein (cerebrospinal fluid)</term><term>tau Proteins (cerebrospinal fluid)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="cerebrospinal fluid" xml:lang="en"><term>Amyloid beta-Peptides</term><term>Peptide Fragments</term><term>alpha-Synuclein</term><term>tau Proteins</term></keywords><keywords scheme="MESH" qualifier="cerebrospinal fluid" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Threonine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Memory</term><term>Movement</term><term>Verbal Learning</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Case-Control Studies</term><term>Cohort Studies</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Phosphorylation</term><term>Regression Analysis</term><term>Severity of Illness Index</term><term>Statistics as Topic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We observed a significant correlation between cerebrospinal fluid (CSF) levels of tau proteins and α-synuclein, but not β-amyloid 1-42 (Aβ1-42), and lower concentration of CSF biomarkers, as compared with healthy controls, in a cohort of entirely untreated patients with Parkinson disease (PD) at the earliest stage of the disease studied so far.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23979011</PMID><DateCreated><Year>2014</Year><Month>02</Month><Day>03</Day></DateCreated><DateCompleted><Year>2014</Year><Month>02</Month><Day>14</Day></DateCompleted><DateRevised><Year>2015</Year><Month>05</Month><Day>27</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2168-6157</ISSN><JournalIssue CitedMedium="Internet"><Volume>70</Volume><Issue>10</Issue><PubDate><Year>2013</Year><Month>Oct</Month></PubDate></JournalIssue><Title>JAMA neurology</Title><ISOAbbreviation>JAMA Neurol</ISOAbbreviation></Journal><ArticleTitle>Association of cerebrospinal fluid β-amyloid 1-42, T-tau, P-tau181, and α-synuclein levels with clinical features of drug-naive patients with early Parkinson disease.</ArticleTitle><Pagination><MedlinePgn>1277-87</MedlinePgn></Pagination><Abstract><AbstractText Label="IMPORTANCE" NlmCategory="OBJECTIVE">We observed a significant correlation between cerebrospinal fluid (CSF) levels of tau proteins and α-synuclein, but not β-amyloid 1-42 (Aβ1-42), and lower concentration of CSF biomarkers, as compared with healthy controls, in a cohort of entirely untreated patients with Parkinson disease (PD) at the earliest stage of the disease studied so far.</AbstractText><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">To evaluate the baseline characteristics and relationship to clinical features of CSF biomarkers (Aβ1-42, total tau [T-tau], tau phosphorylated at threonine 181 [P-tau181], and α-synuclein) in drug-naive patients with early PD and demographically matched healthy controls enrolled in the Parkinson's Progression Markers Initiative (PPMI) study.</AbstractText><AbstractText Label="DESIGN, SETTING, AND PARTICIPANTS" NlmCategory="METHODS">Cross-sectional study of the initial 102 research volunteers (63 patients with PD and 39 healthy controls) of the PPMI cohort.</AbstractText><AbstractText Label="MAIN OUTCOMES AND MEASURES" NlmCategory="METHODS">The CSF biomarkers were measured by INNO-BIA AlzBio3 immunoassay (Aβ1-42, T-tau, and P-tau181; Innogenetics Inc) or by enzyme-linked immunosorbent assay (α-synuclein). Clinical features including diagnosis, demographic characteristics, motor, neuropsychiatric, and cognitive assessments, and DaTscan were systematically assessed according to the PPMI study protocol.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Slightly, but significantly, lower levels of Aβ1-42, T-tau, P-tau181, α-synuclein, and T-tau/Aβ1-42 were seen in subjects with PD compared with healthy controls but with a marked overlap between groups. Using multivariate regression analysis, we found that lower Aβ1-42 and P-tau181 levels were associated with PD diagnosis and that decreased CSF T-tau and α-synuclein were associated with increased motor severity. Notably, when we classified patients with PD by their motor phenotypes, lower CSF Aβ1-42 and P-tau181 concentrations were associated with the postural instability-gait disturbance-dominant phenotype but not with the tremor-dominant or intermediate phenotype. Finally, we found a significant correlation of the levels of α-synuclein with the levels of T-tau and P-tau181.</AbstractText><AbstractText Label="CONCLUSIONS AND RELEVANCE" NlmCategory="CONCLUSIONS">In this first report of CSF biomarkers in PPMI study subjects,we found that measures of CSF Aβ1-42, T-tau, P-tau181, and α-synuclein have prognostic and diagnostic potential in early-stage PD. Further investigations using the entire PPMI cohort will test the predictive performance of CSF biomarkers for PD progression</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kang</LastName><ForeName>Ju-Hee</ForeName><Initials>JH</Initials></Author><Author ValidYN="Y"><LastName>Irwin</LastName><ForeName>David J</ForeName><Initials>DJ</Initials></Author><Author ValidYN="Y"><LastName>Chen-Plotkin</LastName><ForeName>Alice S</ForeName><Initials>AS</Initials></Author><Author ValidYN="Y"><LastName>Siderowf</LastName><ForeName>Andrew</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Caspell</LastName><ForeName>Chelsea</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Coffey</LastName><ForeName>Christopher S</ForeName><Initials>CS</Initials></Author><Author ValidYN="Y"><LastName>Waligórska</LastName><ForeName>Teresa</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Taylor</LastName><ForeName>Peggy</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Sarah</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Frasier</LastName><ForeName>Mark</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Marek</LastName><ForeName>Kenneth</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Kieburtz</LastName><ForeName>Karl</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Jennings</LastName><ForeName>Danna</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Simuni</LastName><ForeName>Tanya</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Tanner</LastName><ForeName>Caroline M</ForeName><Initials>CM</Initials></Author><Author ValidYN="Y"><LastName>Singleton</LastName><ForeName>Andrew</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Toga</LastName><ForeName>Arthur W</ForeName><Initials>AW</Initials></Author><Author ValidYN="Y"><LastName>Chowdhury</LastName><ForeName>Sohini</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mollenhauer</LastName><ForeName>Brit</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Trojanowski</LastName><ForeName>John Q</ForeName><Initials>JQ</Initials></Author><Author ValidYN="Y"><LastName>Shaw</LastName><ForeName>Leslie M</ForeName><Initials>LM</Initials></Author><Author ValidYN="Y"><CollectiveName>Parkinson's Progression Markers Initiative</CollectiveName></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>01AG000949-06</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K23MH092735</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS038377</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS053488</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50NS053488-05</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 AG024904</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U01 NS082134</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>Z01 AG000949-03</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>Z01AG000949-06</GrantID><Acronym>AG</Acronym><Agency>NIA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>JAMA Neurol</MedlineTA><NlmUniqueID>101589536</NlmUniqueID><ISSNLinking>2168-6149</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016229">Amyloid beta-Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010446">Peptide Fragments</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051844">alpha-Synuclein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C075222">amyloid beta-protein (1-42)</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016875">tau Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>2ZD004190S</RegistryNumber><NameOfSubstance UI="D013912">Threonine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2009 Apr;65(4):403-13</RefSource><PMID Version="1">19296504</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2009 Sep;23(9):2820-30</RefSource><PMID Version="1">19369384</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 2009 Dec;41(12):1308-12</RefSource><PMID Version="1">19915575</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2009 Nov 15;24(15):2203-10</RefSource><PMID Version="1">19795497</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2010 Mar;133(Pt 3):713-26</RefSource><PMID 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