Publications

Journal Article Research Support, Non-U.S. Gov't Ppublish 22 citations

PubMed: 38323780 DOI: 10.1002/alz.13687

Fully automated measurement of plasma Aβ42/40 and p-tau181: Analytical robustness and concordance with cerebrospinal fluid profile along the Alzheimer's disease continuum in two independent cohorts.

Alzheimers Dement 20(4):2453-2468

Authors: Giovanni Bellomo, Sherif Bayoumy, Alfredo Megaro, Andrea Toja, Giovanna Nardi, Lorenzo Gaetani, Elena R Blujdea, Federico Paolini Paoletti, Anna Lidia Wojdaƚa, Davide Chiasserini, Wiesje M van der Flier, Inge M W Verberk, Charlotte Teunissen, Lucilla Parnetti

Affiliations

  • Center for Memory Disturbances, Lab of Clinical Neurochemistry, Section of Neurology, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.
  • Neurochemistry Laboratory, Department of Laboratory Medicine, Amsterdam Neuroscience, Amsterdam UMC, Amsterdam, The Netherlands.
  • Section of Biochemistry, Department of Medicine and Surgery, University of Perugia, Perugia, Italy.
  • Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
  • Department of Epidemiology and Data Science, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.

Abstract

INTRODUCTION

For routine clinical implementation of Alzheimer's disease (AD) plasma biomarkers, fully automated random-access platforms are crucial to ensure reproducible measurements. We aimed to perform an analytical validation and to establish cutoffs for AD plasma biomarkers measured with Lumipulse.

METHODS

Two cohorts were included. UNIPG: n = 450 paired cerebrospinal fluid (CSF)/plasma samples from subjects along the AD-continuum, subjects affected by other neurodegenerative diseases, and controls with known CSF profile; AMS: n = 40 plasma samples from AD and n = 40 controls. Plasma amyloid β (Aβ)42, Aβ40, and p-tau181 were measured with Lumipulse. We evaluated analytical and diagnostic performance.

RESULTS

Lumipulse assays showed high analytical performance. Plasma p-tau181 levels accurately reflected CSF A+/T+ profile in AD-dementia and mild cognitive impairment (MCI)-AD, but not in asymptomatic-AD. Plasma and CSF Aβ42/40 values were concordant across clinical AD stages. Cutoffs and probability-based models performed satisfactorily in both cohorts.

DISCUSSION

The identified cutoffs and probability-based models represent a significant step toward plasma AD molecular diagnosis.

MeSH

Research Design, Dementia, Alzheimer Disease, Probability, Cognitive Dysfunction, Biomarkers, Plasma

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