Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/24955
Title: Longitudinal evaluation of the natural history of amyloid-β in plasma and brain.
Austin Authors: Burnham, Samantha C;Fandos, Noelia;Fowler, Christopher;Pérez-Grijalba, Virginia;Doré, Vincent ;Doecke, James D;Shishegar, Rosita;Cox, Timothy;Fripp, Jurgen;Rowe, Christopher C ;Sarasa, Manuel;Masters, Colin L ;Pesini, Pedro;Villemagne, Victor L 
Affiliation: Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical Sciences, Edith Cowan University, Joondalup, WA 6027, Australia
The Australian e-Health Research Centre, CSIRO Health & Biosecurity, Parkville, VIC 3052, Australia
Department of Medicine, The University of Melbourne, Parkville, VIC 3052, Australia
The Australian e-Health Research Centre, CSIRO Health and Biosecurity, Herston 4029, Australia
Molecular Imaging and Therapy
The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC 3010, Australia
Araclon Biotech-Grifols, Zaragoza 50009, Spain
Issue Date: Apr-2020
metadata.dc.date: 2020
Publication information: Brain Communications 2020; 2(1): fcaa041
Abstract: Plasma amyloid-β peptide concentration has recently been shown to have high accuracy to predict amyloid-β plaque burden in the brain. These amyloid-β plasma markers will allow wider screening of the population and simplify and reduce screening costs for therapeutic trials in Alzheimer's disease. The aim of this study was to determine how longitudinal changes in blood amyloid-β track with changes in brain amyloid-β. Australian Imaging, Biomarker and Lifestyle study participants with a minimum of two assessments were evaluated (111 cognitively normal, 7 mild cognitively impaired, 15 participants with Alzheimer's disease). Amyloid-β burden in the brain was evaluated through PET and was expressed in Centiloids. Total protein amyloid-β 42/40 plasma ratios were determined using ABtest® assays. We applied our method for obtaining natural history trajectories from short term data to measures of total protein amyloid-β 42/40 plasma ratios and PET amyloid-β. The natural history trajectory of total protein amyloid-β 42/40 plasma ratios appears to approximately mirror that of PET amyloid-β, with both spanning decades. Rates of change of 7.9% and 8.8%, were observed for total protein amyloid-β 42/40 plasma ratios and PET amyloid-β, respectively. The trajectory of plasma amyloid-β preceded that of brain amyloid-β by a median value of 6 years (significant at 88% confidence interval). These findings, showing the tight association between changes in plasma and brain amyloid-β, support the use of plasma total protein amyloid-β 42/40 plasma ratios as a surrogate marker of brain amyloid-β. Also, that plasma total protein amyloid-β 42/40 plasma ratios has potential utility in monitoring trial participants, and as an outcome measure.
URI: https://ahro.austin.org.au/austinjspui/handle/1/24955
DOI: 10.1093/braincomms/fcaa041
ORCID: 0000-0003-2863-0293
PubMed URL: 32954297
Type: Journal Article
Subjects: Alzheimer’s disease
aging
amyloid imaging
plasma amyloid
Appears in Collections:Journal articles

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