Microglia turnover with aging and in an Alzheimer’s model via long-term in vivo single-cell imaging
Abstract
To clarify the role of microglia in brain homeostasis and disease, an understanding of their maintenance, proliferation and turnover is essential. The lifespan of brain microglia, however, remains uncertain, and reflects confounding factors in earlier assessments that were largely indirect. We genetically labeled single resident microglia in living mice and then used multiphoton microscopy to monitor these cells over time. Under homeostatic conditions, we found that neocortical resident microglia were long-lived, with a median lifetime of well over 15 months; thus, approximately half of these cells survive the entire mouse lifespan. While proliferation of resident neocortical microglia under homeostatic conditions was low, microglial proliferation in a mouse model of Alzheimer's β-amyloidosis was increased threefold. The persistence of individual microglia throughout the mouse lifespan provides an explanation for how microglial priming early in life can induce lasting functional changes and how microglial senescence may contribute to age-related neurodegenerative diseases.
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In mouse and human brain, turnover of microglia depends on high proliferation rates spatially coupled to efficient apoptosis to maintain steady state cell numbers in each brain region.
“In mouse and human brain turnover of microglia depends on high proliferation rates spatially coupled to efficient apoptosis in order to maintain steady state cell numbers in each brain region (Askew et al., 2017; Füger et al., 2017).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Füger et al., 2017
Estimates of physiological microglia turnover rate in mice vary from 0.13 to 0.8% across studies.
“the estimated microglia turnover rate ranging from 0.13 to 0.8% (Askew et al., 2017; Füger et al., 2017; Lawson et al., 1992; Tay et al., 2017)”
From Pu.1/Spi1 dosage controls the turnover and maintenance of microglia in zebrafish and mammals (2025) · cites this paper as Füger et al., 2017
In APP/PS1 mice, proliferation of microglia was threefold.
“While turnover of microglia under homeostatic conditions in the brain is low, in APP/PS1 mice proliferation of microglia was threefold [52].”
From Microglia specific deletion of miR-155 in Alzheimer’s disease mouse models reduces amyloid-β pathology but causes hyperexcitability and seizures (2023) · cites this paper as [52]
Microglia live 0.5-3.4 years in the mouse brain and up to 20 years in the human brain.
“Microglia live 0.5–3.4 years in the mouse brain [313] and up to 20 years in the human brain [314].”
From Revisiting the Pathogenesis of X-Linked Adrenoleukodystrophy (2025) · cites this paper as [313]
Microglia divide at an extremely low rate at older ages.
“suggesting that microglia divide at an extremely low rate at older ages, an assertion supported by recent publications (Fuger et al., 2017).”
From Complex cell-state changes revealed by single cell RNA sequencing of 76,149 microglia throughout the mouse lifespan and in the injured brain (2018) · cites this paper as Fuger et al., 2017
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“…yielded distinct or even contradictory results i.e., the estimated microglia turnover rate ranging from 0.13 to 0.8% (Askew, Li et al., 2017, Füger, Hefendehl et al., 2017, Lawson, Perry et al., 1992, Tay, Mai et al., 2017), which indicated that microglia in adult mice (~2 years lifespan)…”
Influential
- Authors
- Füger, P., Hefendehl, J. K., Veeraraghavalu, K., Wendeln, A.-C., Schlosser, C., Obermüller, U., Wegenast-Braun, B. M., Neher, J. J., Martus, P., Kohsaka, S., Thunemann, M., Feil, R., Sisodia, S. S., Skodras, A., & Jucker, M.
- Affiliations
- German Center for Neurodegenerative Diseases (DE)
- University of Chicago (US)
- Hertie Institute for Clinical Brain Research (DE)
- University of Tübingen (DE)
- National Institute of Neuroscience (JP)
- Corresponding author
- Skodras, Angelos
- Jucker, Mathias
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2017-08-28
- Volume
- 20
- Issue
- 10
- Pages
- 1371-1376
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2747817360
- Cited by
- 401
- References
- 38
- Citations by year
- 2026: 24 · 2025: 42 · 2024: 56 · 2023: 47 · 2022: 39 · 2021: 66 · 2020: 39 · 2019: 39 · 2018: 38 · 2017: 11
- FWCI
- 17.30
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion)
- Funders
- National Institute on Aging (R01AG027854, R01AG021494)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- microglia, microglial proliferation, Alzheimer's disease, beta-amyloidosis, microglial senescence, microglial priming, aging, mouse model
- MeSH terms
- Aging, Alzheimer Disease, Animals, Mice, Transgenic, Cell Death, Microglia, Neocortex, Microscopy, Fluorescence, Multiphoton, Cell Proliferation, Mice, Kaplan-Meier Estimate, Plaque, Amyloid, Single-Cell Analysis
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