Differential pattern of brain‐specific CSF proteins tau and amyloid‐beta in Parkinsonian syndromes
Identifieur interne : 002184 ( Main/Merge ); précédent : 002183; suivant : 002185Differential pattern of brain‐specific CSF proteins tau and amyloid‐beta in Parkinsonian syndromes
Auteurs : Sigurd D. Süssmuth [Allemagne] ; Ingo Uttner [Allemagne] ; Bernhard Landwehrmeyer [Allemagne] ; Elmar H. Pinkhardt [Allemagne] ; Johannes Brettschneider [Allemagne] ; Axel Petzold [Royaume-Uni] ; Bernd Kramer [Allemagne] ; Jörg B. Schulz [Allemagne] ; Christian Palm [Allemagne] ; Markus Otto [Allemagne] ; Albert C. Ludolph [Allemagne] ; Jan Kassubek [Allemagne] ; Hayrettin Tumani [Allemagne]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-07-15.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Amyloid beta-Peptides (cerebrospinal fluid), Female, Glial Fibrillary Acidic Protein (cerebrospinal fluid), Humans, Male, Middle Aged, PSP‐P, Parkinsonian Disorders (cerebrospinal fluid), Peptide Fragments (cerebrospinal fluid), Richardson's syndrome, Statistics, Nonparametric, biomarker, cerebrospinal fluid, multiple system atrophy, progressive supranuclear palsy, tau Proteins (cerebrospinal fluid).
- MESH :
- chemical , cerebrospinal fluid : Amyloid beta-Peptides, Glial Fibrillary Acidic Protein, Peptide Fragments, tau Proteins.
- cerebrospinal fluid : Parkinsonian Disorders.
- Adult, Aged, Aged, 80 and over, Female, Humans, Male, Middle Aged, Statistics, Nonparametric.
Abstract
To evaluate cerebrospinal fluid (CSF) proteins reflecting processes of neurodegeneration and glial activation in progressive supranuclear palsy (PSP; Richardson's syndrome, n = 20; PSP‐Parkinsonism, n = 7) and multiple system atrophy (MSA, n = 25), we analyzed tau, phosphorylated tau, amyloid‐beta1–42 (Aβ1–42), Aβ1–40, glial fibrillary acidic protein (GFAP), and CSF routine variables. Individuals with PSP‐Parkinsonism and MSA had elevated tau levels when compared with Richardson's syndrome, Parkinson's disease (PD), and age‐matched controls (P ≤ 0.001). Ratios of P‐tau/T‐tau were significantly different in Parkinsonian syndromes. CSF Aβ1–42 was decreased only in patients with Richardson's syndrome. In a subset of Parkinsonian syndromes, we found elevated GFAP concentrations and increased CSF/serum albumin ratios. There were no correlations between biomarker concentrations and clinical scores in any of the diseases. In conclusion, this preliminary data show that changes in CSF tau and Aβ1–42 may indicate different protein processing in PSP patients and might, therefore, be relevant in the differentiation of PSP subtypes. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22895
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<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Amyloid beta-Peptides (cerebrospinal fluid)</term>
<term>Female</term>
<term>Glial Fibrillary Acidic Protein (cerebrospinal fluid)</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>PSP‐P</term>
<term>Parkinsonian Disorders (cerebrospinal fluid)</term>
<term>Peptide Fragments (cerebrospinal fluid)</term>
<term>Richardson's syndrome</term>
<term>Statistics, Nonparametric</term>
<term>biomarker</term>
<term>cerebrospinal fluid</term>
<term>multiple system atrophy</term>
<term>progressive supranuclear palsy</term>
<term>tau Proteins (cerebrospinal fluid)</term>
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<term>Glial Fibrillary Acidic Protein</term>
<term>Peptide Fragments</term>
<term>tau Proteins</term>
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<keywords scheme="MESH" qualifier="cerebrospinal fluid" xml:lang="en"><term>Parkinsonian Disorders</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Female</term>
<term>Humans</term>
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<front><div type="abstract" xml:lang="en">To evaluate cerebrospinal fluid (CSF) proteins reflecting processes of neurodegeneration and glial activation in progressive supranuclear palsy (PSP; Richardson's syndrome, n = 20; PSP‐Parkinsonism, n = 7) and multiple system atrophy (MSA, n = 25), we analyzed tau, phosphorylated tau, amyloid‐beta1–42 (Aβ1–42), Aβ1–40, glial fibrillary acidic protein (GFAP), and CSF routine variables. Individuals with PSP‐Parkinsonism and MSA had elevated tau levels when compared with Richardson's syndrome, Parkinson's disease (PD), and age‐matched controls (P ≤ 0.001). Ratios of P‐tau/T‐tau were significantly different in Parkinsonian syndromes. CSF Aβ1–42 was decreased only in patients with Richardson's syndrome. In a subset of Parkinsonian syndromes, we found elevated GFAP concentrations and increased CSF/serum albumin ratios. There were no correlations between biomarker concentrations and clinical scores in any of the diseases. In conclusion, this preliminary data show that changes in CSF tau and Aβ1–42 may indicate different protein processing in PSP patients and might, therefore, be relevant in the differentiation of PSP subtypes. © 2010 Movement Disorder Society</div>
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</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Brettschneider, Johannes" sort="Brettschneider, Johannes" uniqKey="Brettschneider J" first="Johannes" last="Brettschneider">Johannes Brettschneider</name>
<affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Petzold, Axel" sort="Petzold, Axel" uniqKey="Petzold A" first="Axel" last="Petzold">Axel Petzold</name>
<affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Deparment of Neuroimmunology, Institute of Neurology, Queen Square, London</wicri:regionArea>
<placeName><settlement type="city">Londres</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Grand Londres</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Kramer, Bernd" sort="Kramer, Bernd" uniqKey="Kramer B" first="Bernd" last="Kramer">Bernd Kramer</name>
<affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Schulz, Jorg B" sort="Schulz, Jorg B" uniqKey="Schulz J" first="Jörg B." last="Schulz">Jörg B. Schulz</name>
<affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurodegeneration and Restorative Research, Center for Neurological Medicine, University of Göttingen, Göttingen</wicri:regionArea>
<placeName><region type="land" nuts="2">Basse-Saxe</region>
<settlement type="city">Göttingen</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Palm, Christian" sort="Palm, Christian" uniqKey="Palm C" first="Christian" last="Palm">Christian Palm</name>
<affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Otto, Markus" sort="Otto, Markus" uniqKey="Otto M" first="Markus" last="Otto">Markus Otto</name>
<affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Ludolph, Albert C" sort="Ludolph, Albert C" uniqKey="Ludolph A" first="Albert C." last="Ludolph">Albert C. Ludolph</name>
<affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Kassubek, Jan" sort="Kassubek, Jan" uniqKey="Kassubek J" first="Jan" last="Kassubek">Jan Kassubek</name>
<affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Tumani, Hayrettin" sort="Tumani, Hayrettin" uniqKey="Tumani H" first="Hayrettin" last="Tumani">Hayrettin Tumani</name>
<affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Movement Disorders</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2010-07-15">2010-07-15</date>
<biblScope unit="vol">25</biblScope>
<biblScope unit="issue">9</biblScope>
<biblScope unit="page" from="1284">1284</biblScope>
<biblScope unit="page" to="1288">1288</biblScope>
</imprint>
<idno type="ISSN">0885-3185</idno>
</series>
<idno type="istex">E06A7675ED6F9BC2A578724A87C6A31F18A5977C</idno>
<idno type="DOI">10.1002/mds.22895</idno>
<idno type="ArticleID">MDS22895</idno>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PSP‐P</term>
<term>Richardson's syndrome</term>
<term>biomarker</term>
<term>cerebrospinal fluid</term>
<term>multiple system atrophy</term>
<term>progressive supranuclear palsy</term>
</keywords>
</textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">To evaluate cerebrospinal fluid (CSF) proteins reflecting processes of neurodegeneration and glial activation in progressive supranuclear palsy (PSP; Richardson's syndrome, n = 20; PSP‐Parkinsonism, n = 7) and multiple system atrophy (MSA, n = 25), we analyzed tau, phosphorylated tau, amyloid‐beta1–42 (Aβ1–42), Aβ1–40, glial fibrillary acidic protein (GFAP), and CSF routine variables. Individuals with PSP‐Parkinsonism and MSA had elevated tau levels when compared with Richardson's syndrome, Parkinson's disease (PD), and age‐matched controls (P ≤ 0.001). Ratios of P‐tau/T‐tau were significantly different in Parkinsonian syndromes. CSF Aβ1–42 was decreased only in patients with Richardson's syndrome. In a subset of Parkinsonian syndromes, we found elevated GFAP concentrations and increased CSF/serum albumin ratios. There were no correlations between biomarker concentrations and clinical scores in any of the diseases. In conclusion, this preliminary data show that changes in CSF tau and Aβ1–42 may indicate different protein processing in PSP patients and might, therefore, be relevant in the differentiation of PSP subtypes. © 2010 Movement Disorder Society</div>
</front>
</TEI>
</ISTEX>
<PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Differential pattern of brain-specific CSF proteins tau and amyloid-β in Parkinsonian syndromes.</title>
<author><name sortKey="Sussmuth, Sigurd D" sort="Sussmuth, Sigurd D" uniqKey="Sussmuth S" first="Sigurd D" last="Süssmuth">Sigurd D. Süssmuth</name>
<affiliation wicri:level="4"><nlm:affiliation>Department of Neurology, University of Ulm, Ulm, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Uttner, Ingo" sort="Uttner, Ingo" uniqKey="Uttner I" first="Ingo" last="Uttner">Ingo Uttner</name>
</author>
<author><name sortKey="Landwehrmeyer, Bernhard" sort="Landwehrmeyer, Bernhard" uniqKey="Landwehrmeyer B" first="Bernhard" last="Landwehrmeyer">Bernhard Landwehrmeyer</name>
</author>
<author><name sortKey="Pinkhardt, Elmar H" sort="Pinkhardt, Elmar H" uniqKey="Pinkhardt E" first="Elmar H" last="Pinkhardt">Elmar H. Pinkhardt</name>
</author>
<author><name sortKey="Brettschneider, Johannes" sort="Brettschneider, Johannes" uniqKey="Brettschneider J" first="Johannes" last="Brettschneider">Johannes Brettschneider</name>
</author>
<author><name sortKey="Petzold, Axel" sort="Petzold, Axel" uniqKey="Petzold A" first="Axel" last="Petzold">Axel Petzold</name>
</author>
<author><name sortKey="Kramer, Bernd" sort="Kramer, Bernd" uniqKey="Kramer B" first="Bernd" last="Kramer">Bernd Kramer</name>
</author>
<author><name sortKey="Schulz, Jorg B" sort="Schulz, Jorg B" uniqKey="Schulz J" first="Jörg B" last="Schulz">Jörg B. Schulz</name>
</author>
<author><name sortKey="Palm, Christian" sort="Palm, Christian" uniqKey="Palm C" first="Christian" last="Palm">Christian Palm</name>
</author>
<author><name sortKey="Otto, Markus" sort="Otto, Markus" uniqKey="Otto M" first="Markus" last="Otto">Markus Otto</name>
</author>
<author><name sortKey="Ludolph, Albert C" sort="Ludolph, Albert C" uniqKey="Ludolph A" first="Albert C" last="Ludolph">Albert C. Ludolph</name>
</author>
<author><name sortKey="Kassubek, Jan" sort="Kassubek, Jan" uniqKey="Kassubek J" first="Jan" last="Kassubek">Jan Kassubek</name>
</author>
<author><name sortKey="Tumani, Hayrettin" sort="Tumani, Hayrettin" uniqKey="Tumani H" first="Hayrettin" last="Tumani">Hayrettin Tumani</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2010">2010</date>
<idno type="doi">10.1002/mds.22895</idno>
<idno type="RBID">pubmed:20589870</idno>
<idno type="pmid">20589870</idno>
<idno type="wicri:Area/PubMed/Corpus">001786</idno>
<idno type="wicri:Area/PubMed/Curation">001786</idno>
<idno type="wicri:Area/PubMed/Checkpoint">001940</idno>
<idno type="wicri:Area/Ncbi/Merge">002C31</idno>
<idno type="wicri:Area/Ncbi/Curation">002C31</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">002C31</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Differential pattern of brain-specific CSF proteins tau and amyloid-β in Parkinsonian syndromes.</title>
<author><name sortKey="Sussmuth, Sigurd D" sort="Sussmuth, Sigurd D" uniqKey="Sussmuth S" first="Sigurd D" last="Süssmuth">Sigurd D. Süssmuth</name>
<affiliation wicri:level="4"><nlm:affiliation>Department of Neurology, University of Ulm, Ulm, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Neurology, University of Ulm, Ulm</wicri:regionArea>
<placeName><region type="land" nuts="1">Bade-Wurtemberg</region>
<region type="district" nuts="2">District de Tübingen</region>
<settlement type="city">Ulm</settlement>
</placeName>
<orgName type="university">Université d'Ulm</orgName>
</affiliation>
</author>
<author><name sortKey="Uttner, Ingo" sort="Uttner, Ingo" uniqKey="Uttner I" first="Ingo" last="Uttner">Ingo Uttner</name>
</author>
<author><name sortKey="Landwehrmeyer, Bernhard" sort="Landwehrmeyer, Bernhard" uniqKey="Landwehrmeyer B" first="Bernhard" last="Landwehrmeyer">Bernhard Landwehrmeyer</name>
</author>
<author><name sortKey="Pinkhardt, Elmar H" sort="Pinkhardt, Elmar H" uniqKey="Pinkhardt E" first="Elmar H" last="Pinkhardt">Elmar H. Pinkhardt</name>
</author>
<author><name sortKey="Brettschneider, Johannes" sort="Brettschneider, Johannes" uniqKey="Brettschneider J" first="Johannes" last="Brettschneider">Johannes Brettschneider</name>
</author>
<author><name sortKey="Petzold, Axel" sort="Petzold, Axel" uniqKey="Petzold A" first="Axel" last="Petzold">Axel Petzold</name>
</author>
<author><name sortKey="Kramer, Bernd" sort="Kramer, Bernd" uniqKey="Kramer B" first="Bernd" last="Kramer">Bernd Kramer</name>
</author>
<author><name sortKey="Schulz, Jorg B" sort="Schulz, Jorg B" uniqKey="Schulz J" first="Jörg B" last="Schulz">Jörg B. Schulz</name>
</author>
<author><name sortKey="Palm, Christian" sort="Palm, Christian" uniqKey="Palm C" first="Christian" last="Palm">Christian Palm</name>
</author>
<author><name sortKey="Otto, Markus" sort="Otto, Markus" uniqKey="Otto M" first="Markus" last="Otto">Markus Otto</name>
</author>
<author><name sortKey="Ludolph, Albert C" sort="Ludolph, Albert C" uniqKey="Ludolph A" first="Albert C" last="Ludolph">Albert C. Ludolph</name>
</author>
<author><name sortKey="Kassubek, Jan" sort="Kassubek, Jan" uniqKey="Kassubek J" first="Jan" last="Kassubek">Jan Kassubek</name>
</author>
<author><name sortKey="Tumani, Hayrettin" sort="Tumani, Hayrettin" uniqKey="Tumani H" first="Hayrettin" last="Tumani">Hayrettin Tumani</name>
</author>
</analytic>
<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="eISSN">1531-8257</idno>
<imprint><date when="2010" type="published">2010</date>
</imprint>
</series>
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</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Amyloid beta-Peptides (cerebrospinal fluid)</term>
<term>Female</term>
<term>Glial Fibrillary Acidic Protein (cerebrospinal fluid)</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Parkinsonian Disorders (cerebrospinal fluid)</term>
<term>Peptide Fragments (cerebrospinal fluid)</term>
<term>Statistics, Nonparametric</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>Glial Fibrillary Acidic Protein</term>
<term>Peptide Fragments</term>
<term>tau Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="cerebrospinal fluid" xml:lang="en"><term>Parkinsonian Disorders</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Statistics, Nonparametric</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">To evaluate cerebrospinal fluid (CSF) proteins reflecting processes of neurodegeneration and glial activation in progressive supranuclear palsy (PSP; Richardson's syndrome, n = 20; PSP-Parkinsonism, n = 7) and multiple system atrophy (MSA, n = 25), we analyzed tau, phosphorylated tau, amyloid-beta(1-42) (Abeta1-42), Abeta1-40, glial fibrillary acidic protein (GFAP), and CSF routine variables. Individuals with PSP-Parkinsonism and MSA had elevated tau levels when compared with Richardson's syndrome, Parkinson's disease (PD), and age-matched controls (P </div>
</front>
</TEI>
</PubMed>
</double>
</record>
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