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Ultrasensitive Detection of Plasma Amyloid-beta as a Biomarker for Cognitively Normal Elderly Individuals at Risk of Alzheimer's Disease

Journal article
Authors P. Chatterjee
M. Elmi
K. Goozee
T. Shah
H. R. Sohrabi
C. B. Dias
S. Pedrini
K. Shen
P. R. Asih
P. Dave
K. Taddei
H. Vanderstichele
Henrik Zetterberg
Kaj Blennow
R. N. Martins
Published in Journal of Alzheimers Disease
Volume 71
Issue 3
Pages 775-783
ISSN 1387-2877
Publication year 2019
Published at Institute of Neuroscience and Physiology
Pages 775-783
Language en
Links dx.doi.org/10.3233/jad-190533
Keywords Alzheimer's disease, blood biomarkers, plasma amyloid-beta, plasma amyloid-beta ratios, preclinical, dementia, quantification, association, deposition, decline, Neurosciences & Neurology, lstein mf, 1975, journal of psychiatric research, v12, p189, lvikoski t, 1995, new england journal of medicine, v333, p1242
Subject categories Neurology

Abstract

Background: Aberrant amyloid-beta (A beta) deposition in the brain occurs two decades prior to the manifestation of Alzheimer's disease (AD) clinical symptoms and therefore brain A beta load measured using PET serves as a gold standard biomarker for the early diagnosis of AD. However, the uneconomical nature of PET makes blood markers, that reflect brain A beta deposition, attractive candidates for investigation as surrogate markers. Objective: Investigation of plasma A beta as a surrogate marker for brain A beta deposition in cognitively normal elderly individuals. Methods: Plasma A beta(40) and A beta(42) concentrations were measured using the ultrasensitive Single Molecule Array (Simoa) assay in 95 cognitively normal elderly individuals, who have all undergone PET to assess brain A beta deposition. Based on the standard uptake value ratios (SUVR) obtained from PET imaging, using the tracer F-18-Florbetaben, plasma A beta was compared between 32 participants assessed to have low brain A beta load (A beta-, SUVR <1.35) and 63 assessed to have high brain A beta load (A beta+, SUVR >= 1.35). Results: Plasma A beta(42)/A beta(40) ratios were lower in the A beta+ group compared to the A beta- group. Plasma A beta(40) and A beta(42) levels were not significantly different between A beta- and A beta+ groups, although a trend of higher plasma A beta(40) was observed in the A beta+ group. Additionally, plasma A beta(42)/A beta(40) ratios along with the known AD risk factors, age and APOE epsilon 4 status, resulted in A beta+ participants being distinguished from A beta- participants based on an area under the receiver operating characteristic curve shown to be 78%. Conclusion: Plasma A beta ratios in this study are a potential biomarker for brain A beta deposition and therefore, for preclinical AD. However, this method to measure plasma A beta needs further development to increase the accuracy of this promising AD blood biomarker.

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