Browsing by Author "Korecka, Magdalena"

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    The Alzheimer's Disease Neuroimaging Initiative 2 Biomarker Core: A review of progress and plans
    (Elsevier, 2015-07) Kang, Ju-Hee; Korecka, Magdalena; Figurski, Michal J.; Toledo, Jon B.; Blennow, Kaj; Zetterberg, Henrik; Waligorska, Teresa; Brylska, Magdalena; Fields, Leona; Shah, Nirali; Soares, Holly; Dean, Robert A.; Vanderstichele, Hugo; Petersen, Ronald C.; Aisen, Paul S.; Saykin, Andrew J.; Weiner, Michael W.; Trojanowski, John Q.; Shaw, Leslie M.; Alzheimer's Disease Neuroimaging Initiative; Department of Radiology and Imaging Sciences, School of Medicine
    INTRODUCTION: We describe Alzheimer's Disease Neuroimaging Initiative (ADNI) Biomarker Core progress including: the Biobank; cerebrospinal fluid (CSF) amyloid beta (Aβ1-42), t-tau, and p-tau181 analytical performance, definition of Alzheimer's disease (AD) profile for plaque, and tangle burden detection and increased risk for progression to AD; AD disease heterogeneity; progress in standardization; and new studies using ADNI biofluids. METHODS: Review publications authored or coauthored by ADNI Biomarker core faculty and selected non-ADNI studies to deepen the understanding and interpretation of CSF Aβ1-42, t-tau, and p-tau181 data. RESULTS: CSF AD biomarker measurements with the qualified AlzBio3 immunoassay detects neuropathologic AD hallmarks in preclinical and prodromal disease stages, based on CSF studies in non-ADNI living subjects followed by the autopsy confirmation of AD. Collaboration across ADNI cores generated the temporal ordering model of AD biomarkers varying across individuals because of genetic/environmental factors that increase/decrease resilience to AD pathologies. DISCUSSION: Further studies will refine this model and enable the use of biomarkers studied in ADNI clinically and in disease-modifying therapeutic trials.
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    The global Alzheimer's Association round robin study on plasma amyloid β methods
    (Wiley, 2021-10-14) Pannee, Josef; Shaw, Leslie M.; Korecka, Magdalena; Waligorska, Teresa; Teunissen, Charlotte E.; Stoops, Erik; Vanderstichele, Hugo M. J.; Mauroo, Kimberley; Verberk, Inge M. W.; Keshavan, Ashvini; Pesini, Pedro; Sarasa, Leticia; Pascual-Lucas, Maria; Fandos, Noelia; Allué, José-Antonio; Portelius, Erik; Andreasson, Ulf; Yoda, Ritsuko; Nakamura, Akinori; Kaneko, Naoki; Yang, Shieh-Yueh; Liu, Huei-Chun; Palme, Stefan; Bittner, Tobias; Mawuenyega, Kwasi G.; Ovod, Vitaliy; Bollinger, James; Bateman, Randall J.; Li, Yan; Dage, Jeffrey L.; Stomrud, Erik; Hansson, Oskar; Schott, Jonathan M.; Blennow, Kaj; Zetterberg, Henrik; Neurology, School of Medicine
    Introduction: Blood-based assays to measure brain amyloid beta (Aβ) deposition are an attractive alternative to the cerebrospinal fluid (CSF)-based assays currently used in clinical settings. In this study, we examined different blood-based assays to measure Aβ and how they compare among centers and assays. Methods: Aliquots from 81 plasma samples were distributed to 10 participating centers. Seven immunological assays and four mass-spectrometric methods were used to measure plasma Aβ concentrations. Results: Correlations were weak for Aβ42 while Aβ40 correlations were stronger. The ratio Aβ42/Aβ40 did not improve the correlations and showed weak correlations. Discussion: The poor correlations for Aβ42 in plasma might have several potential explanations, such as the high levels of plasma proteins (compared to CSF), sensitivity to pre-analytical sample handling and specificity, and cross-reactivity of different antibodies. Different methods might also measure different pools of plasma Aβ42. We, however, hypothesize that greater correlations might be seen in future studies because many of the methods have been refined during completion of this study.