Serveur d'exploration sur la maladie de Parkinson

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CSF Aβ42 and tau in Parkinson's disease with cognitive impairment

Identifieur interne : 000792 ( Main/Exploration ); précédent : 000791; suivant : 000793

CSF Aβ42 and tau in Parkinson's disease with cognitive impairment

Auteurs : Thomas J. Montine [États-Unis] ; Min Shi [États-Unis] ; Joseph F. Quinn [États-Unis] ; Elaine R. Peskind [États-Unis] ; Suzanne Craft [États-Unis] ; Carmen Ginghina [États-Unis] ; Kathryn A. Chung [États-Unis] ; Hojoong Kim [États-Unis] ; Douglas R. Galasko [États-Unis] ; Joseph Jankovic [États-Unis] ; Cyrus P. Zabetian [États-Unis] ; James B. Leverenz [États-Unis] ; Jing Zhang [États-Unis]

Source :

RBID : ISTEX:E22F3584401FA8AF62FC70D3542C9D9107AC3FA8

English descriptors

Abstract

We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P < 0.05) and PD‐D (P < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society

Url:
DOI: 10.1002/mds.23287


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

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<div type="abstract" xml:lang="en">We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P < 0.05) and PD‐D (P < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society</div>
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<name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name>
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