Please use this identifier to cite or link to this item:
Title: Innate phagocytosis by peripheral blood monocytes is altered in Alzheimer's disease
Austin Authors: Gu, Ben J;Huang, Xin;Ou, Amber;Rembach, Alan;Fowler, Christopher J;Avula, Pavan K;Horton, Adam;Doecke, James D;Villemagne, Victor L ;Macaulay, S Lance;Maruff, Paul;Fletcher, Erica L;Guymer, Robyn;Wiley, James S;Masters, Colin L ;The Australian Imaging, Biomarkers and Lifestyle (AIBL) Study
Affiliation: Department of Nuclear Medicine and Centre for PET, Austin Health, Heidelberg, Victoria, Australia
The Florey Institute of Neuroscience & Mental Health, The University of Melbourne, Parkville, Victoria, Australia
CSIRO Health and Biosecurity/Australian E-Health Research Centre, Herston, Queensland, Australia
CSIRO Health and Biosecurity, Parkville, Victoria, Australia
Cogstate Pty Ltd, Melbourne, Victoria, Australia
Department of Anatomy and Neuroscience, The University of Melbourne, Parkville, Victoria, Australia
Centre for Eye Research Australia Royal Victorian Eye and Ear Hospital, The University of Melbourne, East Melbourne, Victoria, Australia
Issue Date: Sep-2016 2016-07-13
Publication information: Acta Neuropathologica 2016; 132(3): 377-89
Abstract: Sporadic Alzheimer's disease (AD) is characterised by the deposition and accumulation of specific protein aggregates. Failure of clearance could underlie this process, and recent genetic association studies point towards involvement of the phagocytosis and autophagy pathways. We developed a real-time tri-color flow cytometry method to quantitate the phagocytic function of human peripheral blood monocyte subsets including non-classic CD14(dim)CD16(+), intermediate CD14(+)CD16(+) and classic CD14(+)CD16(-) monocytes. Using this method, we have measured the phagocytic ability of fresh monocytes in a study of preclinical, prodromal and clinical AD, matched with cognitively normal healthy control subjects. Basal levels of phagocytosis in all three subsets of monocytes were similar between healthy controls and AD patients, while a significant increase of basal phagocytosis was found in subjects with high Aβ-amyloid burden as assessed by PET scans. Pre-treating cells with Copaxone (CPX, to stimulate phagocytosis) or ATP (an inhibitor of P2X7-mediated phagocytosis) showed a differential response depending on clinical or Aβ-burden status, indicating a relative functional deficit. Overall the results are consistent with a perturbation of basal and stimulated innate phagocytosis in sporadic AD.
DOI: 10.1007/s00401-016-1596-3
Journal: Acta Neuropathologica
PubMed URL:
Type: Journal Article
Subjects: ATP
Alzheimer’s disease
Copaxone (glatiramer acetate)
Appears in Collections:Journal articles

Show full item record

Page view(s)

checked on Jan 27, 2023

Google ScholarTM


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.