The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Microglial senescence: does the brain's immune system have an expiration date?
Abstract
Microglia are seen as the sentries in the CNS who provide a first line of defense whenever there is injury or disease. Microglia and related perivascular macrophages perform various functions, ranging from immunological surveillance to neuroprotection. Recent work in the aged human brain has provided morphological evidence of structural deterioration of microglia, and work in rodents suggests that microglia are subject to replicative senescence (loss of mitotic ability after repeated rounds of replication). Together these observations raise the possibility that old age, and perhaps other factors (genetic and epigenetic) adversely affect viability and self-renewal capacity of microglia, resulting in the generation of senescent and/or dysfunctional cells. Such attrition of the brain's immune system could contribute to the development of neurodegenerative disease by diminishing glial neuroprotection.
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“The ageing brain is also characterised by structural and functional changes to microglial cells, which are the resident immune cell population of the central nervous system (CNS) and are the CNS equivalent of macrophages. They are activated by brain injury and local and systemic inflammation and become primed (hyper-responsive) to small stimuli with ageing, which can potentially cause damage and”
From Frailty in elderly people (2013) · cites this paper as [27]
In the citing paper
“Aged microglia display a dystrophic phenotype118–120. It is also known that ageing, similar to neurodegeneration, induces a hypersensitive, pro-inflammatory microglial phenotype that some have referred to as ‘primed microglia’26.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [119]
In the citing paper
“References 118 and 119 propose that microglial senescence is important for age-related decline in cognitive function.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [119]
Citations
Cites
Microglia: a sensor for pathological events in the CNS
Kreutzberg, G. W. (1996) · Trends in Neurosciences · doi:10.1016/0166-2236(96)10049-7 · Cited by 4,396
Perivascular microglial cells of the CNS are bone marrow-derived and present antigen in vivo
Hickey, W. F., & Kimura, H. (1988) · Science · doi:10.1126/science.3276004 · Cited by 1,466
Simard, A. R., Soulet, D., Gowing, G., Julien, J.-P., & Rivest, S. (2006) · Neuron · doi:10.1016/j.neuron.2006.01.022 · Cited by 1,265
Streit, W. J., Walter, S. A., & Pennell, N. A. (1999) · Progress in Neurobiology · doi:10.1016/s0301-0082(98)00069-0 · Cited by 1,096
Self-citationMicroglia as neuroprotective, immunocompetent cells of the CNS
Streit, W. J. (2002) · Glia · doi:10.1002/glia.10154 · Cited by 919
Self-citationTurnover of resident microglia in the normal adult mouse brain
Lawson, L. J., Perry, V. H., & Gordon, S. (1992) · Neuroscience · doi:10.1016/0306-4522(92)90500-2 · Cited by 709
Dystrophic microglia in the aging human brain
Streit, W. J., Sammons, N. W., Kuhns, A. J., & Sparks, D. L. (2004) · Glia · doi:10.1002/glia.10319 · Cited by 705
Self-citationPriller, J., Flügel, A., Wehner, T., Boentert, M., Haas, C. A., Prinz, M., Fernández-Klett, F., Prass, K., Bechmann, I., de Boer, B. A., et al. (2001) · Nature Medicine · doi:10.1038/nm1201-1356 · Cited by 637
Lectin binding by resting and reactive microglia
Streit, W. J., & Kreutzberg, G. W. (1987) · Journal of Neurocytology · doi:10.1007/bf01795308 · Cited by 496
Self-citationAmeboid microglia as effectors of inflammation in the central nervous system
Giulian, D. (1987) · Journal of Neuroscience Research · doi:10.1002/jnr.490180123 · Cited by 482
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Clegg, A., Young, J., Iliffe, S., Rikkert, M. O., & Rockwood, K. (2013) · The Lancet · doi:10.1016/s0140-6736(12)62167-9 · Cited by 9,503
Microglia: Active sensor and versatile effector cells in the normal and pathologic brain
Hanisch, U.-K., & Kettenmann, H. (2007) · Nature Neuroscience · doi:10.1038/nn1997 · Cited by 3,676
Kettenmann, H., Hanisch, U.-K., Noda, M., & Verkhratsky, A. (2011) · Physiological Reviews · doi:10.1152/physrev.00011.2010 · Cited by 3,547
Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?
Leng, F., & Edison, P. (2021) · Nature Reviews Neurology · doi:10.1038/s41582-020-00435-y · Cited by 3,179
Microglia in neurodegenerative disease
Perry, V. H., Nicoll, J. A. R., & Holmes, C. (2010) · Nature Reviews Neurology · doi:10.1038/nrneurol.2010.17 · Cited by 1,543
Metadata
- Authors
- Streit, W. J.
- Affiliations
- University of Florida Health (US)
- Corresponding author
- Streit, Wolfgang J.
- ORCID
- Streit, Wolfgang J.
- Venue
- Trends in Neurosciences
- Publisher
- Elsevier BV
- Published
- 2006-09
- Volume
- 29
- Issue
- 9
- Pages
- 506-510
- ISSN
- 0166-2236 (ISSN-L)
- OpenAlex
- W1981310043
- Cited by
- 397
- References
- 42
- Citations by year
- 2026: 4 · 2025: 12 · 2024: 10 · 2023: 15 · 2022: 15 · 2021: 18 · 2020: 22 · 2019: 21 · 2018: 18 · 2017: 18 · 2016: 26 · 2015: 22 · 2014: 23 · 2013: 20 · 2012: 40
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- microglial senescence, replicative senescence, microglia, perivascular macrophages, brain aging, neuroinflammation, neuroprotection, neurodegenerative diseases, immunosenescence
- MeSH terms
- Aging, Animals, Brain, Humans, Cellular Senescence, Microglia
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