CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study
Identifieur interne : 001110 ( Main/Corpus ); précédent : 001109; suivant : 001111CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study
Auteurs : Guido Alves ; Kolbj Rn Br Nnick ; Dag Aarsland ; Kaj Blennow ; Henrik Zetterberg ; Clive Ballard ; Martin Wilhelm Kurz ; Ulf Andreasson ; Ole-Bj Rn Tysnes ; Jan Petter Larsen ; Ezra MulugetaSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2010-10.
Abstract
Background Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD. Methods CSF concentrations of Aβ42, Aβ40 and Aβ38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD. Results PD patients displayed significant reductions in Aβ42 (19%; p=0.009), Aβ40 (15.5%; p=0.008) and Aβ38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Aβ42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Aβ42 (β=0.205; p=0.019), Aβ40 (β=0.378; p<0.001) and Aβ38 (β=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures. Conclusion CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Aβ protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Aβ peptides as prognostic biomarkers in PD.
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DOI: 10.1136/jnnp.2009.199950
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Sweden</mods:affiliation></affiliation></author><author><name sortKey="Ballard, Clive" sort="Ballard, Clive" uniqKey="Ballard C" first="Clive" last="Ballard">Clive Ballard</name><affiliation><mods:affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Kurz, Martin Wilhelm" sort="Kurz, Martin Wilhelm" uniqKey="Kurz M" first="Martin Wilhelm" last="Kurz">Martin Wilhelm Kurz</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation></author><author><name sortKey="Andreasson, Ulf" sort="Andreasson, Ulf" uniqKey="Andreasson U" first="Ulf" last="Andreasson">Ulf Andreasson</name><affiliation><mods:affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Tysnes, Ole Bj Rn" sort="Tysnes, Ole Bj Rn" uniqKey="Tysnes O" first="Ole-Bj Rn" last="Tysnes">Ole-Bj Rn Tysnes</name><affiliation><mods:affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</mods:affiliation></affiliation></author><author><name sortKey="Larsen, Jan Petter" sort="Larsen, Jan Petter" uniqKey="Larsen J" first="Jan Petter" last="Larsen">Jan Petter Larsen</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</mods:affiliation></affiliation></author><author><name sortKey="Mulugeta, Ezra" sort="Mulugeta, Ezra" uniqKey="Mulugeta E" first="Ezra" last="Mulugeta">Ezra Mulugeta</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:D9A88C5545460E8836F1C8A7681C92D546EAA8D0</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1136/jnnp.2009.199950</idno><idno type="url">https://api.istex.fr/document/D9A88C5545460E8836F1C8A7681C92D546EAA8D0/fulltext/pdf</idno><idno 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Hospital, Stavanger, Norway</mods:affiliation></affiliation></author><author><name sortKey="Aarsland, Dag" sort="Aarsland, Dag" uniqKey="Aarsland D" first="Dag" last="Aarsland">Dag Aarsland</name><affiliation><mods:affiliation>Department of Psychiatry, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation></author><author><name sortKey="Blennow, Kaj" sort="Blennow, Kaj" uniqKey="Blennow K" first="Kaj" last="Blennow">Kaj Blennow</name><affiliation><mods:affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Zetterberg, Henrik" sort="Zetterberg, Henrik" uniqKey="Zetterberg H" first="Henrik" last="Zetterberg">Henrik Zetterberg</name><affiliation><mods:affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Ballard, Clive" sort="Ballard, Clive" uniqKey="Ballard C" first="Clive" last="Ballard">Clive Ballard</name><affiliation><mods:affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Kurz, Martin Wilhelm" sort="Kurz, Martin Wilhelm" uniqKey="Kurz M" first="Martin Wilhelm" last="Kurz">Martin Wilhelm Kurz</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation></author><author><name sortKey="Andreasson, Ulf" sort="Andreasson, Ulf" uniqKey="Andreasson U" first="Ulf" last="Andreasson">Ulf Andreasson</name><affiliation><mods:affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Tysnes, Ole Bj Rn" sort="Tysnes, Ole Bj Rn" uniqKey="Tysnes O" first="Ole-Bj Rn" last="Tysnes">Ole-Bj Rn Tysnes</name><affiliation><mods:affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</mods:affiliation></affiliation></author><author><name sortKey="Larsen, Jan Petter" sort="Larsen, Jan Petter" uniqKey="Larsen J" first="Jan Petter" last="Larsen">Jan Petter Larsen</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</mods:affiliation></affiliation></author><author><name sortKey="Mulugeta, Ezra" sort="Mulugeta, Ezra" uniqKey="Mulugeta E" first="Ezra" last="Mulugeta">Ezra Mulugeta</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="ISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2010-10">2010-10</date><biblScope unit="volume">81</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1080">1080</biblScope></imprint><idno type="ISSN">0022-3050</idno></series><idno type="istex">D9A88C5545460E8836F1C8A7681C92D546EAA8D0</idno><idno type="DOI">10.1136/jnnp.2009.199950</idno><idno type="href">jnnp-81-1080.pdf</idno><idno type="ArticleID">jnnp199950</idno><idno type="PMID">20547614</idno><idno type="local">jnnp;81/10/1080</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3050</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD. Methods CSF concentrations of Aβ42, Aβ40 and Aβ38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD. Results PD patients displayed significant reductions in Aβ42 (19%; p=0.009), Aβ40 (15.5%; p=0.008) and Aβ38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Aβ42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Aβ42 (β=0.205; p=0.019), Aβ40 (β=0.378; p<0.001) and Aβ38 (β=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures. Conclusion CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Aβ protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Aβ peptides as prognostic biomarkers in PD.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>Guido Alves</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>E-mail: algu@sus.no</json:string></affiliations></json:item><json:item><name>Kolbjørn Brønnick</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string></affiliations></json:item><json:item><name>Dag Aarsland</name><affiliations><json:string>Department of Psychiatry, Stavanger University Hospital, Stavanger, Norway</json:string></affiliations></json:item><json:item><name>Kaj Blennow</name><affiliations><json:string>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</json:string></affiliations></json:item><json:item><name>Henrik Zetterberg</name><affiliations><json:string>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</json:string></affiliations></json:item><json:item><name>Clive Ballard</name><affiliations><json:string>Wolfson Centre for Age Related Diseases, King's College, London, UK</json:string></affiliations></json:item><json:item><name>Martin Wilhelm Kurz</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</json:string></affiliations></json:item><json:item><name>Ulf Andreasson</name><affiliations><json:string>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</json:string></affiliations></json:item><json:item><name>Ole-Bjørn Tysnes</name><affiliations><json:string>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</json:string><json:string>Department of Neurology, Haukeland University Hospital, Bergen, Norway</json:string></affiliations></json:item><json:item><name>Jan Petter Larsen</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</json:string></affiliations></json:item><json:item><name>Ezra Mulugeta</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>Wolfson Centre for Age Related Diseases, King's College, London, UK</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Research paper</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cerebrospinal fluid (CSF)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>biomarkers</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cognition</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurobiology</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Background Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD. Methods CSF concentrations of Aβ42, Aβ40 and Aβ38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD. Results PD patients displayed significant reductions in Aβ42 (19%; p=0.009), Aβ40 (15.5%; p=0.008) and Aβ38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Aβ42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Aβ42 (β=0.205; p=0.019), Aβ40 (β=0.378; p>0.001) and Aβ38 (β=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures. Conclusion CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Aβ protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Aβ peptides as prognostic biomarkers in PD.</abstract><qualityIndicators><score>8.493</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595.276 x 793.701 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1823</abstractCharCount><pdfWordCount>4993</pdfWordCount><pdfCharCount>34386</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>260</abstractWordCount></qualityIndicators><title>CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study</title><pmid><json:string>20547614</json:string></pmid><genre><json:string>research-article</json:string></genre><host><volume>81</volume><pages><first>1080</first></pages><issn><json:string>0022-3050</json:string></issn><issue>10</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-330X</json:string></eissn><title>Journal of Neurology, Neurosurgery & 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Publishing Group Ltd</publisher><availability><p>BMJ</p></availability><date>2010-06-14</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study</title><author corresp="yes"><persName><forename type="first">Guido</forename><surname>Alves</surname></persName><email>algu@sus.no</email><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation></author><author><persName><forename type="first">Kolbjørn</forename><surname>Brønnick</surname></persName><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation></author><author><persName><forename type="first">Dag</forename><surname>Aarsland</surname></persName><affiliation>Department of Psychiatry, Stavanger University Hospital, Stavanger, Norway</affiliation></author><author><persName><forename type="first">Kaj</forename><surname>Blennow</surname></persName><affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation></author><author><persName><forename type="first">Henrik</forename><surname>Zetterberg</surname></persName><affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation></author><author><persName><forename type="first">Clive</forename><surname>Ballard</surname></persName><affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</affiliation></author><author><persName><forename type="first">Martin Wilhelm</forename><surname>Kurz</surname></persName><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation></author><author><persName><forename type="first">Ulf</forename><surname>Andreasson</surname></persName><affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation></author><author><persName><forename type="first">Ole-Bjørn</forename><surname>Tysnes</surname></persName><affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</affiliation><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation></author><author><persName><forename type="first">Jan Petter</forename><surname>Larsen</surname></persName><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</affiliation></author><author><persName><forename type="first">Ezra</forename><surname>Mulugeta</surname></persName><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</affiliation></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2010-10"></date><biblScope unit="volume">81</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1080">1080</biblScope></imprint></monogr><idno type="istex">D9A88C5545460E8836F1C8A7681C92D546EAA8D0</idno><idno type="DOI">10.1136/jnnp.2009.199950</idno><idno type="href">jnnp-81-1080.pdf</idno><idno type="ArticleID">jnnp199950</idno><idno type="PMID">20547614</idno><idno type="local">jnnp;81/10/1080</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010-06-14</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Background Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD. Methods CSF concentrations of Aβ42, Aβ40 and Aβ38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD. Results PD patients displayed significant reductions in Aβ42 (19%; p=0.009), Aβ40 (15.5%; p=0.008) and Aβ38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Aβ42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Aβ42 (β=0.205; p=0.019), Aβ40 (β=0.378; p<0.001) and Aβ38 (β=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures. Conclusion CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Aβ protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Aβ peptides as prognostic biomarkers in PD.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Alzheimer's disease</term></item><item><term>cerebrospinal fluid (CSF)</term></item><item><term>biomarkers</term></item><item><term>cognition</term></item><item><term>neurobiology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-06-14">Created</change><change when="2010-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D9A88C5545460E8836F1C8A7681C92D546EAA8D0/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-id journal-id-type="publisher-id">jnnp</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><abbrev-journal-title>J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">jnnp199950</article-id><article-id pub-id-type="doi">10.1136/jnnp.2009.199950</article-id><article-id pub-id-type="other">jnnp;81/10/1080</article-id><article-id pub-id-type="other">jnnp;jnnp.2009.199950</article-id><article-id pub-id-type="pmid">20547614</article-id><article-id pub-id-type="other">1080</article-id><article-id pub-id-type="other">jnnp.2009.199950</article-id><article-categories><subj-group subj-group-type="heading"><subject content-type="original">Research paper</subject></subj-group></article-categories><title-group><article-title>CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study</article-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Alves</surname><given-names>Guido</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Brønnick</surname><given-names>Kolbjørn</given-names></name><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Aarsland</surname><given-names>Dag</given-names></name><xref ref-type="aff" rid="aff3">3</xref></contrib><contrib contrib-type="author"><name><surname>Blennow</surname><given-names>Kaj</given-names></name><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Zetterberg</surname><given-names>Henrik</given-names></name><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Ballard</surname><given-names>Clive</given-names></name><xref ref-type="aff" rid="aff5">5</xref></contrib><contrib contrib-type="author"><name><surname>Kurz</surname><given-names>Martin Wilhelm</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author"><name><surname>Andreasson</surname><given-names>Ulf</given-names></name><xref ref-type="aff" rid="aff4">4</xref></contrib><contrib contrib-type="author"><name><surname>Tysnes</surname><given-names>Ole-Bjørn</given-names></name><xref ref-type="aff" rid="aff6">6</xref><xref ref-type="aff" rid="aff7">7</xref></contrib><contrib contrib-type="author"><name><surname>Larsen</surname><given-names>Jan Petter</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref><xref ref-type="aff" rid="aff6">6</xref></contrib><contrib contrib-type="author"><name><surname>Mulugeta</surname><given-names>Ezra</given-names></name><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff5">5</xref></contrib></contrib-group><aff id="aff1"><label>1</label>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</aff><aff id="aff2"><label>2</label>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</aff><aff id="aff3"><label>3</label>Department of Psychiatry, Stavanger University Hospital, Stavanger, Norway</aff><aff id="aff4"><label>4</label>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</aff><aff id="aff5"><label>5</label>Wolfson Centre for Age Related Diseases, King's College, London, UK</aff><aff id="aff6"><label>6</label>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</aff><aff id="aff7"><label>7</label>Department of Neurology, Haukeland University Hospital, Bergen, Norway</aff><author-notes><corresp><label>Correspondence to</label> Dr Guido Alves, The Norwegian Centre for Movement Disorders, Stavanger University Hospital, PO Box 8100 N-4068 Stavanger, Norway; <email>algu@sus.no</email></corresp></author-notes><pub-date pub-type="epub-original"><day>14</day><month>6</month><year>2010</year></pub-date><pub-date pub-type="ppub"><month>10</month><year>2010</year></pub-date><pub-date pub-type="epub"><day>14</day><month>6</month><year>2010</year></pub-date><volume>81</volume><volume-id pub-id-type="other">81</volume-id><volume-id pub-id-type="other">81</volume-id><issue>10</issue><issue-id pub-id-type="other">jnnp;81/10</issue-id><issue-id pub-id-type="other">10</issue-id><issue-id pub-id-type="other">81/10</issue-id><fpage>1080</fpage><history><date date-type="received"><day>11</day><month>11</month><year>2009</year></date><date date-type="rev-recd"><day>11</day><month>1</month><year>2010</year></date><date date-type="accepted"><day>20</day><month>1</month><year>2010</year></date></history><permissions><copyright-statement>© 2010, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</copyright-statement><copyright-year>2010</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-81-1080.pdf"></self-uri><abstract><sec><title>Background</title><p>Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD.</p></sec><sec><title>Methods</title><p>CSF concentrations of Aβ42, Aβ40 and Aβ38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD.</p></sec><sec><title>Results</title><p>PD patients displayed significant reductions in Aβ42 (19%; p=0.009), Aβ40 (15.5%; p=0.008) and Aβ38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Aβ42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Aβ42 (β=0.205; p=0.019), Aβ40 (β=0.378; p<0.001) and Aβ38 (β=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures.</p></sec><sec><title>Conclusion</title><p>CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Aβ protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Aβ peptides as prognostic biomarkers in PD.</p></sec></abstract><kwd-group><kwd>Parkinson's disease</kwd><kwd>Alzheimer's disease</kwd><kwd>cerebrospinal fluid (CSF)</kwd><kwd>biomarkers</kwd><kwd>cognition</kwd><kwd>neurobiology</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Guido</namePart><namePart type="family">Alves</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>E-mail: algu@sus.no</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kolbjørn</namePart><namePart type="family">Brønnick</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Dag</namePart><namePart type="family">Aarsland</namePart><affiliation>Department of Psychiatry, Stavanger University Hospital, Stavanger, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kaj</namePart><namePart type="family">Blennow</namePart><affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Henrik</namePart><namePart type="family">Zetterberg</namePart><affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Clive</namePart><namePart type="family">Ballard</namePart><affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martin Wilhelm</namePart><namePart type="family">Kurz</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ulf</namePart><namePart type="family">Andreasson</namePart><affiliation>Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ole-Bjørn</namePart><namePart type="family">Tysnes</namePart><affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</affiliation><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jan Petter</namePart><namePart type="family">Larsen</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Institute of Clinical Medicine, University of Bergen, Bergen, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ezra</namePart><namePart type="family">Mulugeta</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Wolfson Centre for Age Related Diseases, King's College, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2010-10</dateIssued><dateCreated encoding="w3cdtf">2010-06-14</dateCreated><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Background Alzheimer's disease (AD) pathology is found in a considerable portion of patients with Parkinson's disease (PD), particularly those with early dementia (PDD). Altered cerebrospinal fluid (CSF) levels of amyloid-β (Aβ) and tau proteins have been found in PDD, with intermediate changes for Aβ42 in non-demented PD. The authors investigated whether AD-related CSF protein levels are altered and relate to neuropsychological performance in early, untreated PD. Methods CSF concentrations of Aβ42, Aβ40 and Aβ38 were measured by electrochemiluminiscene and levels of total tau (T-tau) and phosphorylated tau (P-tau) by ELISA in 109 newly diagnosed, unmedicated, non-demented, community-based PD patients who had undergone comprehensive neuropsychological testing, and were compared with those of 36 age-matched normal controls and 20 subjects with mild AD. Results PD patients displayed significant reductions in Aβ42 (19%; p=0.009), Aβ40 (15.5%; p=0.008) and Aβ38 (23%; p=0.004) but not T-tau (p=0.816) or P-tau (p=0.531) compared with controls. CSF Aβ42 reductions in PD were less marked than in AD (53%; p=0.002). Sequential regression analyses demonstrated significant associations between CSF levels of Aβ42 (β=0.205; p=0.019), Aβ40 (β=0.378; p<0.001) and Aβ38 (β=0.288; p=0.001) and memory impairment, but not executive-attentional or visuospatial dysfunction. Tau protein levels did not correlate with cognitive measures. Conclusion CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. Our study suggests that alterations in Aβ protein metabolism may contribute to the heterogeneity in pattern and course of cognitive decline associated with PD. Longitudinal studies are needed to clarify the clinical significance of CSF Aβ peptides as prognostic biomarkers in PD.</abstract><subject><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Alzheimer's disease</topic><topic>cerebrospinal fluid (CSF)</topic><topic>biomarkers</topic><topic>cognition</topic><topic>neurobiology</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID">jnnp</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>81</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1080</start></extent></part></relatedItem><identifier type="istex">D9A88C5545460E8836F1C8A7681C92D546EAA8D0</identifier><identifier type="DOI">10.1136/jnnp.2009.199950</identifier><identifier type="href">jnnp-81-1080.pdf</identifier><identifier type="ArticleID">jnnp199950</identifier><identifier type="PMID">20547614</identifier><identifier type="local">jnnp;81/10/1080</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010, Published by the BMJ Publishing Group Limited. 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