Profiling Microglia From Alzheimer’s Disease Donors and Non-demented Elderly in Acute Human Postmortem Cortical Tissue
Alsema, Astrid M.; Jiang, Qiong; Kracht, Laura; Gerrits, Emma; Dubbelaar, Marissa L.; Miedema, Anneke; Brouwer, Nieske; Hol, Elly M.; Middeldorp, Jinte; van Dijk, Roland; Woodbury, Maya; Wachter, Astrid; Xi, Simon; Möller, Thomas; Biber, Knut P.; Kooistra, Susanne M.; Boddeke, Erik W.G.M.; Eggen, Bart J.L.
(2020) Frontiers in Molecular Neuroscience, volume 13, pp. 1 - 14
(Article)
Abstract
Microglia are the tissue-resident macrophages of the central nervous system (CNS). Recent studies based on bulk and single-cell RNA sequencing in mice indicate high relevance of microglia with respect to risk genes and neuro-inflammation in Alzheimer’s disease (AD). Here, we investigated microglia transcriptomes at bulk and single-cell levels in non-demented
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elderly and AD donors using acute human postmortem cortical brain samples. We identified seven human microglial subpopulations with heterogeneity in gene expression. Notably, gene expression profiles and subcluster composition of microglia did not differ between AD donors and non-demented elderly in bulk RNA sequencing nor in single-cell sequencing.
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Keywords: Alzheimer’s disease, barcoded Smart-seq2, human, microglia, single-cell RNA sequencing, Alzheimer, s disease, Cellular and Molecular Neuroscience, Molecular Biology, Journal Article
ISSN: 1662-5099
Publisher: Frontiers Media S. A.
Note: Funding Information: We thank the Netherlands Brain Bank and the NeuroBiobank of the Institute Born-Bunge, Belgium. We thank M. Borggrewe, J. Villamil Ortiz, T. Oshima, M. Wijering, S. Eskandar, R. van der Pijl, E. Wesseling, C. Grit, and C. B. Haas for assistance and/or maintenance of sample processing and bulk and/or single-cell isolations. We are grateful to W. Abdulahad, G. Mesander, T. Bijma, and J. Teunis from The Central Flowcytometry Unit of the University of Groningen, University Medical Center Groningen (UMCG), for technical assistance on FACS sorting. We thank P. van der Vlies, D. Brandenburg, N. Festen, and W. Uniken Venema for their assistance setting up the bc-SmartSeq2 protocol. We thank M. Meijer for ICT-related support. We appreciate sequencing-related advice provided by D. Spierings, K. Hoekstra-Wakker, J. Beenen, and N. Halsema. Funding. MW, SX, AW, TM, and KB are employed by AbbVie, Inc., which has subsidized the study. BE acquired funding from the foundation Alzheimer Nederland. EH, EB, and BE received funding from ZonMW-Memorabel. AA and EG are funded by Abbvie. AA was supported by the Jan Kornelis de Cock-Hadders foundation. QJ was funded by the Li Ka-shing Foundation at Shantou University Medical College, China, the Abel Tasman Talent Program, University Medical Center Groningen/University of Groningen, The Netherlands, and the Graduate School of Medical Sciences (GSMS), University of Groningen, The Netherlands. LK holds a scholarship from the GSMS, University of Groningen, The Netherlands. Funding Information: MW, SX, AW, TM, and KB are employed by AbbVie, Inc., which has subsidized the study. BE acquired funding from the foundation Alzheimer Nederland. EH, EB, and BE received funding from ZonMW-Memorabel. AA and EG are funded by Abbvie. AA was supported by the Jan Kornelis de Cock-Hadders foundation. QJ was funded by the Li Ka-shing Foundation at Shantou University Medical College, China, the Abel Tasman Talent Program, University Medical Center Groningen/University of Groningen, The Netherlands, and the Graduate School of Medical Sciences (GSMS), University of Groningen, The Netherlands. LK holds a scholarship from the GSMS, University of Groningen, The Netherlands. Publisher Copyright: © Copyright © 2020 Alsema, Jiang, Kracht, Gerrits, Dubbelaar, Miedema, Brouwer, Hol, Middeldorp, van Dijk, Woodbury, Wachter, Xi, Möller, Biber, Kooistra, Boddeke and Eggen.
(Peer reviewed)
