Brain inflammation and adult neurogenesis: The dual role of microglia
Abstract
In the adult mammalian brain, neurogenesis from neural stem/progenitor cells continues in two regions: the subgranular zone in the dentate gyrus and the subventricular zone lining the lateral ventricles. The generated neuroblasts migrate to their appropriate location and differentiate to mature granule cells and olfactory bulb interneurons, respectively. Following injury such as stroke, neuroblasts generated in the subventricular zone migrate also into areas which are not normally neurogenic, e.g. striatum and cerebral cortex. In the initial studies in rodents, brain inflammation and microglia activation were found to be detrimental for the survival of the new hippocampal neurons early after they had been born. The role of inflammation for adult neurogenesis has, however, turned out to be much more complex. Recent experimental evidence indicates that microglia under certain circumstances can be beneficial and support the different steps in neurogenesis, progenitor proliferation, survival, migration, and differentiation. Here we summarize the current knowledge on the role of inflammation and in particular of microglia in adult neurogenesis in the intact and injured mammalian brain. We conclude that microglia activation, as an indicator of inflammation, is not pro- or antineurogenic per se but the net outcome is dependent on the balance between secreted molecules with pro- and antiinflammatory action.
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Chronic stress activates brain microglia, which secrete cytokines and in turn affect neurogenesis; neurogenesis is either inhibited or stimulated according to the level of microglia activation.
“Chronic stress activates brain microglia, which secrete cytokines and in turn affect neurogenesis. Neurogenesis is either inhibited or stimulated according to the level of microglia activation[52].”
From Neuroinflammation and cytokine abnormality in major depression: cause or consequence in that illness? (2016) · cites this paper as [52]
Activated microglial cells increase in number up to 16 weeks after two-hour MCAO in rats.
“Ekdahl and colleagues reported an increased number of activated microglial cells up to 16 weeks after two hour MCAO in rats (Ekdahl et al., 2009).”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Ekdahl et al., 2009
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- Authors
- Ekdahl, C. T., Kokaia, Z., & Lindvall, O.
- Affiliations
- Lund University (SE)
- Corresponding author
- Ekdahl, C.T.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2009-02
- Volume
- 158
- Issue
- 3
- Pages
- 1021-1029
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W2031809301
- Cited by
- 801
- References
- 89
- Citations by year
- 2026: 10 · 2025: 25 · 2024: 16 · 2023: 33 · 2022: 33 · 2021: 44 · 2020: 41 · 2019: 40 · 2018: 41 · 2017: 34 · 2016: 64 · 2015: 58 · 2014: 75 · 2013: 65 · 2012: 75
- FWCI
- 3.46
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
- Keywords
- adult neurogenesis, microglia, neuroinflammation, microglial activation, subventricular zone, dentate gyrus, neural stem/progenitor cells, neuroblast migration, stroke, hippocampal neurogenesis, olfactory bulb interneurons
- MeSH terms
- Animals, Cell Communication, Encephalitis, Gliosis, Humans, Nerve Regeneration, Neuronal Plasticity, Cytokines, Microglia, Stroke, Neurogenesis
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