CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study
Identifieur interne : 000481 ( Main/Exploration ); précédent : 000480; suivant : 000482CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's Disease: the Norwegian ParkWest study
Auteurs : Guido Alves [Norvège] ; Kolbj Rn Br Nnick [Norvège] ; Dag Aarsland [Norvège] ; Kaj Blennow [Suède] ; Henrik Zetterberg [Suède] ; Clive Ballard [Royaume-Uni] ; Martin Wilhelm Kurz [Norvège] ; Ulf Andreasson [Suède] ; Ole-Bj Rn Tysnes [Norvège] ; Jan Petter Larsen [Norvège] ; Ezra Mulugeta [Norvège, Royaume-Uni]Source :
- 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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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><affiliations><list><country><li>Norvège</li><li>Royaume-Uni</li><li>Suède</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Norvège"><noRegion><name sortKey="Alves, Guido" sort="Alves, Guido" uniqKey="Alves G" first="Guido" last="Alves">Guido Alves</name></noRegion><name sortKey="Aarsland, Dag" sort="Aarsland, Dag" uniqKey="Aarsland D" first="Dag" last="Aarsland">Dag Aarsland</name><name sortKey="Alves, Guido" sort="Alves, Guido" uniqKey="Alves G" first="Guido" last="Alves">Guido Alves</name><name sortKey="Alves, Guido" sort="Alves, Guido" uniqKey="Alves G" first="Guido" last="Alves">Guido Alves</name><name sortKey="Br Nnick, Kolbj Rn" sort="Br Nnick, Kolbj Rn" uniqKey="Br Nnick K" first="Kolbj Rn" last="Br Nnick">Kolbj Rn Br Nnick</name><name sortKey="Kurz, Martin Wilhelm" sort="Kurz, Martin Wilhelm" uniqKey="Kurz M" first="Martin Wilhelm" last="Kurz">Martin Wilhelm Kurz</name><name sortKey="Kurz, Martin Wilhelm" sort="Kurz, Martin Wilhelm" uniqKey="Kurz M" first="Martin Wilhelm" last="Kurz">Martin Wilhelm Kurz</name><name sortKey="Larsen, Jan Petter" sort="Larsen, Jan Petter" uniqKey="Larsen J" first="Jan Petter" last="Larsen">Jan Petter Larsen</name><name sortKey="Larsen, Jan Petter" sort="Larsen, Jan Petter" uniqKey="Larsen J" first="Jan Petter" last="Larsen">Jan Petter Larsen</name><name sortKey="Larsen, Jan Petter" sort="Larsen, Jan Petter" uniqKey="Larsen J" first="Jan Petter" last="Larsen">Jan Petter Larsen</name><name sortKey="Mulugeta, Ezra" sort="Mulugeta, Ezra" uniqKey="Mulugeta E" first="Ezra" last="Mulugeta">Ezra Mulugeta</name><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><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></country><country name="Suède"><noRegion><name sortKey="Blennow, Kaj" sort="Blennow, Kaj" uniqKey="Blennow K" first="Kaj" last="Blennow">Kaj Blennow</name></noRegion><name sortKey="Andreasson, Ulf" sort="Andreasson, Ulf" uniqKey="Andreasson U" first="Ulf" last="Andreasson">Ulf Andreasson</name><name sortKey="Zetterberg, Henrik" sort="Zetterberg, Henrik" uniqKey="Zetterberg H" first="Henrik" last="Zetterberg">Henrik Zetterberg</name></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Ballard, Clive" sort="Ballard, Clive" uniqKey="Ballard C" first="Clive" last="Ballard">Clive Ballard</name></region><name sortKey="Mulugeta, Ezra" sort="Mulugeta, Ezra" uniqKey="Mulugeta E" first="Ezra" last="Mulugeta">Ezra Mulugeta</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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