Annals of Clinical Biochemistry >
Volume 46, Number 3 >
Pp. 235-240
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1 Department of Clinical Chemistry;
2 Department of Neurology, VU University Medical Center, Amsterdam, 1081 HV, The Netherlands;
3 Neurochemistry Lab, Möldal Hospital, Möldal, SE-431 80, Sweden;
4 The Penn Ralston Center, University of Pennsylvania, 19104, Philadelphia;
5 UCLA School of Nursing, Los Angeles, CA 90095, USA;
6 Instituut Born-Bunge, University of Antwerp, Antwerp, BE-2610, Belgium;
7 Department of Biochemical Research, University of San Diego, La Jolla, CA 92093, USA;
8 Department of Psychiatry, Alzheimer Memorial Center, University of Munich, München, D-80336, Germany;
9 Department of Psychiatry, School of Medicine and Trinity College Institute of Neuroscience, Trinity College, Dublin 2, Ireland;
10 Molecular Biology, University of Heidelberg, Heidelberg 69120, Germany;
11 Department of Neurology, Eginition Hospital, Athene, 11528, Greece;
12 Department for Public Health/Geriatrics, Uppsala University, Uppsala 751 25, Sweden;
13 Institute for Basic Research in Development Disabilities, New York 10314, USA;
14 Department of Neurology, Ospedale S.M. della Misericordia, Perugia 06122, Italy;
15 Institute of Neurology, Clinical Neurosciences, UCL, London, WC1N 3BG, UK;
16 Department of Neurology, University of Kuopio, 70210 Kuopio, Finland;
17 Unilabs, CH-8021 Zurich, Switzerland;
18 Department of Clinical Chemistry, Akerhus University Hospital, Lorenskog, NO-1478, Norway;
19 Department of Neurology, Erasmus Medical Center, 3015 CE, Rotterdam;
20 Laboratory of Pediatrics and Neurology, Department of Neurology, Radboud University Nijmegen Medical Centre, Donders Centre for Neuroscience, Alzheimer Center, Nijmegen, 6500 HB, The Netherlands;
21 Neurobiology Laboratory, University of Erlangen-Neurenberg, Erlangen, D-91054, Germany;
22 Mayo Clinic, Jacksonville, FL 32092, USA
Corresponding author: NA Verwey, MD, Department of Clinical Chemistry and Neurology, VU University Medical Center, P.O. BOX 7057, Amsterdam 1007 MB, The Netherlands. Email: n.verwey{at}vumc.nl
Background: Different cerebrospinal fluid (CSF) amyloid-beta 1–42 (Aβ1–42), total Tau (Tau) and Tau phosphorylated at threonine 181 (P-Tau) levels are reported, but currently there is a lack of quality control programmes. The aim of this study was to compare the measurements of these CSF biomarkers, between and within centres.
Methods: Three CSF-pool samples were distributed to 13 laboratories in 2004 and the same samples were again distributed to 18 laboratories in 2008. In 2004 six laboratories measured Aβ1–42, Tau and P-Tau and seven laboratories measured one or two of these marker(s) by enzyme-linked immunosorbent assays (ELISAs). In 2008, 12 laboratories measured all three markers, three laboratories measured one or two marker(s) by ELISAs and three laboratories measured the markers by Luminex.
Results: In 2004, the ELISA intercentre coefficients of variance (interCV) were 31%, 21% and 13% for Aβ1–42, Tau and P-Tau, respectively. These were 37%, 16% and 15%, respectively, in 2008. When we restricted the analysis to the Innotest® (N = 13) for Aβ1–42, lower interCV were calculated (22%). The centres that participated in both years (N = 9) showed interCVs of 21%, 15% and 9% and intra-centre coefficients (intraCV) of variance of 25%,18% and 7% in 2008.
Conclusions: The highest variability was found for Aβ1–42. The variabilities for Tau and P-Tau were lower in both years. The centres that participated in both years showed a high intraCV comparable to their interCV, indicating that there is not only a high variation between but also within centres. Besides a uniform standardization of (pre)analytical procedures, the same assay should be used to decrease the inter/intracentre variation.
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