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Articles by Marinus A. Blankenstein
Total Records ( 4 ) for Marinus A. Blankenstein
  Niklas Mattsson , Ulf Andreasson , Staffan Persson , Hiroyuki Arai , Sat Dev Batish , Sergio Bernardini , Luisella Bocchio- Chiavetto , Marinus A. Blankenstein , Maria C. Carrillo , Sonia Chalbot , Els Coart , Davide Chiasserini , Neal Cutler , Gunilla Dahlfors , Stefan Duller , Anne M. Fagan , Orestes Forlenza , Giovanni B. Frisoni , Douglas Galasko , Daniela Galimberti , Harald Hampel , Aase Handberg , Michael T. Heneka , Adrianna Z. Herskovits , Sanna-Kaisa Herukka , David M. Holtzman , Christian Humpel , Bradley T. Hyman , Khalid Iqbal , Khalid Iqbal , Stephan A. Kaeser , Elmar Kaiser , Elisabeth Kapaki , Daniel Kidd , Peter Klivenyi , Cindy S. Knudsen , Markus P. Kummer , James Lui , Albert Llado , Piotr Lewczuk , Qiao-Xin Li , Ralph Martins , Colin Masters , John McAuliffe , Marc Mercken , Abhay Moghekar , Jose Luis Molinuevo , Thomas J. Montine , William Nowatzke , Richard O’Brien , Markus Otto , George P. Paraskevas , Lucilla Parnetti , Ronald C. Petersen , David Prvulovic , Herman P.M. de Reus , Robert A. Rissman , Elio Scarpini , Alessandro Stefani , Hilkka Soininen , Johannes Schroder , Leslie M. Shaw , Anders Skinningsrud , Brith Skrogstad and Annette Spreer
  Background The cerebrospinal fluid (CSF) biomarkers amyloid β (Aβ)-42, total-tau (T-tau), and phosphorylated-tau (P-tau) demonstrate good diagnostic accuracy for Alzheimer‘s disease (AD). However, there are large variations in biomarker measurements between studies, and between and within laboratories. The Alzheimer‘s Association has initiated a global quality control program to estimate and monitor variability of measurements, quantify batch-to-batch assay variations, and identify sources of variability. In this article, we present the results from the first two rounds of the program. Methods The program is open for laboratories using commercially available kits for Aβ, T-tau, or P-tau. CSF samples (aliquots of pooled CSF) are sent for analysis several times a year from the Clinical Neurochemistry Laboratory at the Molndal campus of the University of Gothenburg, Sweden. Each round consists of three quality control samples. Results Forty laboratories participated. Twenty-six used INNOTEST enzyme-linked immunosorbent assay kits, 14 used Luminex xMAP with the INNO-BIA AlzBio3 kit (both measure Aβ-(1-42), P-tau(181P), and T-tau), and 5 used Meso Scale Discovery with the Aβ triplex (AβN-42, AβN-40, and AβN-38) or T-tau kits. The total coefficients of variation between the laboratories were 13% to 36%. Five laboratories analyzed the samples six times on different occasions. Within-laboratory precisions differed considerably between biomarkers within individual laboratories. Conclusions Measurements of CSF AD biomarkers show large between-laboratory variability, likely caused by factors related to analytical procedures and the analytical kits. Standardization of laboratory procedures and efforts by kit vendors to increase kit performance might lower variability, and will likely increase the usefulness of CSF AD biomarkers.
  Petra E. Spies , Jurgen A.H.R. Claassen , Petronella G.M. Peer , Marinus A. Blankenstein , Charlotte E. Teunissen , Philip Scheltens , Wiesje M. van der Flier , Marcel G.M. Olde Rikkert and Marcel M. Verbeek
  Background We aimed to develop a prediction model based on cerebrospinal fluid (CSF) biomarkers, that would yield a single estimate representing the probability that dementia in a memory clinic patient is due to Alzheimer‘s disease (AD). Methods All patients suspected of dementia in whom the CSF biomarkers had been analyzed were selected from a memory clinic database. Clinical diagnosis was AD (n = 272) or non-AD (n = 289). The prediction model was developed with logistic regression analysis and included CSF amyloid β42, CSF phosphorylated tau181, and sex. Validation was performed on an independent data set from another memory clinic, containing 334 AD and 157 non-AD patients. Results The prediction model estimated the probability that AD is present as follows: p(AD) = 1/(1 + e – [–0.3315 + score]), where score is calculated from –1.9486 × ln(amyloid β42) + 2.7915 × ln(phosphorylated tau181) + 0.9178 × sex (male = 0, female = 1). When applied to the validation data set, the discriminative ability of the model was very good (area under the receiver operating characteristic curve: 0.85). The agreement between the probability of AD predicted by the model and the observed frequency of AD diagnoses was very good after taking into account the difference in AD prevalence between the two memory clinics. Conclusions We developed a prediction model that can accurately predict the probability of AD in a memory clinic population suspected of dementia based on CSF amyloid β42, CSF phosphorylated tau181, and sex.
  Esther L.G.E. Koedam , Annelies E. van der Vlies , Wiesje M. van der Flier , Nicolaas A. Verwey , Ted Koene , Philip Scheltens , Marinus A. Blankenstein and Yolande A.L. Pijnenburg
  Objective In this study we investigated the relationships between cerebrospinal fluid (CSF) biomarkers (tau and amyloid-β1-42 [Aβ1-42]) and cognition or behavior in patients with frontotemporal dementia (the behavioral variant, bvFTD). Methods We included 58 patients with bvFTD. All patients underwent a neuropsychological assessment and lumbar puncture. Relationships between CSF biomarkers and cognition or behavior were assessed with linear regression analysis. Results After correction for age, sex, and education, CSF tau levels were found to be negatively related to the Visual Association Test (standardized β = −0.3, P < .05), whereas CSF Aβ1-42 levels were found to be positively related to the Mini-Mental State Examination (β = 0.3, P < .05), the frontal assessment battery (β = 0.5, P < .05), and digit span backwards test (β = 0.3, P = .01). We did not find relations between CSF biomarkers and behavior (measured by the neuropsychiatric inventory). After excluding all patients with a CSF biomarker profile often seen in Alzheimer‘s disease (high levels of tau and low levels of Aβ1-42), we still found relations between CSF Aβ1-42 levels and Visual Association Test object naming (β = 0.4, P < .05), as well as between CSF Aβ1-42 levels and the frontal assessment battery (β = 0.5, P < .05, but there was no relation between CSF tau and cognition. Conclusion Low CSF Aβ1-42 levels are associated with worse general cognitive function and worse executive function in patients with bvFTD. Our results provide circumstantial evidence for a pathophysiological role of Aβ1-42 in bvFTD.
  Wesley Jongbloed , Maartje I. Kester , Wiesje M. van der Flier , Robert Veerhuis , Philip Scheltens , Marinus A. Blankenstein and Charlotte E. Teunissen
  Background Multiplex assays such as xMAP have been proposed for the assessment of Alzheimer‘s disease (AD) biomarkers amyloid β 42 (Aβ42), tau (Tau), and phosphorylated tau (pTau) in cerebrospinal fluid (CSF). Here, we compared the traditional enzyme-linked immunosorbent assay (ELISA) and xMAP with respect to their: (1) absolute biomarker concentration, (2) ability to distinguish AD from nondemented subjects, (3) ability to monitor AD longitudinally, and (4) ability to predict progression from mild cognitive impairment (MCI) to AD. Methods We selected 68 AD, 62 MCI, and 24 nondemented subjects, performed clinical examinations, and obtained CSF at baseline and 2 years later. Aβ42, Tau, and pTau were measured with both ELISA and xMAP. Results Biomarker levels differed considerably between the two assays, and the differences were concentration dependent. No differences were observed in ability to distinguish nondemented subjects from AD patients between ELISA (area under curve of 0.84 for Aβ42, 0.79 for Tau, and 0.75 for pTau) and xMAP (area under curve of 0.82 for Aβ42, 0.75 for Tau, and 0.73 for pTau), all P < .05. Increased Aβ42 levels of AD patients at follow-up compared with baseline were detected with ELISA, whereas increased Tau levels for nondemented subjects and MCI patients were only detected with xMAP. The hazard ratios for progression from MCI to AD did not differ between the assays. Conclusion Both ELISA and multiplex assays can be used to measure AD biomarker levels in CSF to support clinical diagnosis and predict progression from MCI to AD with similar accuracy. Importantly, the assays‘ output in absolute biomarker concentrations is remarkably different, and this discrepancy cannot be reconciled with simple correction factors.
 
 
 
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