Unique microglia recovery population revealed by single-cell RNAseq following neurodegeneration
Tay TL, Sagar , Dautzenberg J, Gruen D, Prinz M (2018)
Publication Type: Journal article
Publication year: 2018
Journal
Book Volume: 6
Pages Range: 87-
Journal Issue: 1
DOI: 10.1186/s40478-018-0584-3
Abstract
Microglia are brain immune cells that constantly survey their environment to maintain homeostasis. Enhanced microglial reactivity and proliferation are typical hallmarks of neurodegenerative diseases. Whether specific disease-linked microglial subsets exist during the entire course of neurodegeneration, including the recovery phase, is currently unclear. Taking a single-cell RNA-sequencing approach in a susceptibility gene-free model of nerve injury, we identified a microglial subpopulation that upon acute neurodegeneration shares a conserved gene regulatory profile compared to previously reported chronic and destructive neurodegeneration transgenic mouse models. Our data also revealed rapid shifts in gene regulation that defined microglial subsets at peak and resolution of neurodegeneration. Finally, our discovery of a unique transient microglial subpopulation at the onset of recovery may provide novel targets for modulating microglia-mediated restoration of brain health.
Involved external institutions
Albert-Ludwigs-Universität Freiburg
Germany (DE)
Max-Planck-Institut für Immunbiologie und Epigenetik (MPI-IE) / Max Planck Institute of Immunobiology and Epigenetics
Germany (DE)
Germany (DE)
Max-Planck-Institut für Immunbiologie und Epigenetik (MPI-IE) / Max Planck Institute of Immunobiology and Epigenetics
Germany (DE)
How to cite
APA:
Tay, T.L., Sagar, ., Dautzenberg, J., Gruen, D., & Prinz, M. (2018). Unique microglia recovery population revealed by single-cell RNAseq following neurodegeneration. Acta Neuropathologica Communications, 6(1), 87-. https://doi.org/10.1186/s40478-018-0584-3
MLA:
Tay, Tuan Leng, et al. "Unique microglia recovery population revealed by single-cell RNAseq following neurodegeneration." Acta Neuropathologica Communications 6.1 (2018): 87-.
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