The DOI matches its Crossref record; 57 of the 58 references it cites were found in a registry or an index.
Microglia regulate hippocampal neurogenesis during chronic neurodegeneration
Open accessAbstract
Neurogenesis is altered in neurodegenerative disorders, partly regulated by inflammatory factors. We have investigated whether microglia, the innate immune brain cells, regulate hippocampal neurogenesis in neurodegeneration. Using the ME7 model of prion disease we applied gain- or loss-of CSF1R function, as means to stimulate or inhibit microglial proliferation, respectively, to dissect the contribution of these cells to neurogenesis. We found that increased hippocampal neurogenesis correlates with the expansion of the microglia population. The selective inhibition of microglial proliferation caused a reduction in neurogenesis and a restoration of normal neuronal differentiation, supporting a pro-neurogenic role for microglia. Using a gene screening strategy, we identified TGFβ as a molecule controlling the microglial pro-neurogenic response in chronic neurodegeneration, supported by loss-of-function mechanistic experiments. By the selective targeting of microglial proliferation we have been able to uncover a pro-neurogenic role for microglia in chronic neurodegeneration, suggesting promising therapeutic targets to normalise the neurogenic niche during neurodegeneration.
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“Microgliosis and astrocytosis were previously described in the dentate gyrus area of the hippocampus of prion disease mice [32, 38, 39].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [38]
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“pharmacological modulation of microglia with another CSF1R inhibitor, GW2580 was able to reduce neuronal population and aberrant neurogenesis and restore the normal neuronal differentiation [38].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“However, CSF1R is not known to be expressed in neurons [38].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [38]
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In the citing paper
“pharmacological modulation of microglia with another CSF1R inhibitor, GW2580 was able to reduce neuronal population and aberrant neurogenesis and restore the normal neuronal differentiation [38].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [38]
The cited source says what the claim attributes to it.
In the citing paper
“pharmacological modulation of microglia with another CSF1R inhibitor, GW2580 was able to reduce neuronal population and aberrant neurogenesis and restore the normal neuronal differentiation [38].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [38]
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Cites
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Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies
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Inflammatory Blockade Restores Adult Hippocampal Neurogenesis
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Inflammation is detrimental for neurogenesis in adult brain
Ekdahl, C. T., Claasen, J.-H., Bonde, S., Kokaia, Z., & Lindvall, O. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2234031100 · Cited by 1,559
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Peripheral Infusion of IGF-I Selectively Induces Neurogenesis in the Adult Rat Hippocampus
Åberg, M. A. I., Åberg, N. D., Hedbäcker, H., Oscarsson, J., & Eriksson, P. S. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-08-02896.2000 · Cited by 852
Brain inflammation and adult neurogenesis: The dual role of microglia
Ekdahl, C. T., Kokaia, Z., & Lindvall, O. (2009) · Neuroscience · doi:10.1016/j.neuroscience.2008.06.052 · Cited by 801
Bett, A. J., Haddara, W. M. R., PREVEC, L., & Graham, F. L. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.19.8802 · Cited by 742
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Items 101–110 of 110
Dey, R. K., Kumari, R., Ansari, J. A., Patnaik, S., & Ghosh, D. (2025) · Toxicology International · doi:10.18311/ti/2025/v32i1/45957
Vicente‐Rodríguez, M., Mancuso, R., Peris-Yague, A., Simmons, C., Gómez‐Nicola, D., Perry, V. H., Turkheimer, F., Lovestone, S., Parker, C. A., & Cash, D. (2024) · Figshare · doi:10.6084/m9.figshare.26581280
Self-citationJiang, X., Yi, S., Liu, Q., Su, D., Li, L., Xiao, C., & Zhang, J. (2022) · Figshare · doi:10.6084/m9.figshare.19863054
Hippocampal plasticity underlying learning and memory processes in healthy and diseased conditions
Petsophonsakul, P. (2017) · theses.fr (ABES) · doi:10.70675/5fdda64ez871dz42c8za517zf44c3618705e
Angelim, M. K. S. C. (2017) · theses.fr (ABES) · doi:10.70675/2f402166z8a8bz4e47z93c4z20ae8f982074
Physiopathologie et modulation de l’activation microgliale secondaire au sepsis
Verdonk, F. (2016) · theses.fr (ABES) · doi:10.70675/8d3a9e0ez15f7z446bzb0e4z56e24e61058a
Cellular state transitions in neuroimmune disorders
Naffaa, M. M. (2026) · Exploration of Immunology · doi:10.37349/ei.2026.1003261
Landwehr, A., Cools-Lartigue, C., Hadera, V., Bobotis, B. C., Khakpour, M., Gomes, F. V., & Tremblay, M. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.09.24.753926
Camoglio, C., Dedoni, S., Scherma, M., Siddi, C., Nilsson, I. A. K., & Fadda, P. (2026) · Physiology & Behavior · doi:10.1016/j.physbeh.2026.115542
Metadata
- Authors
- De Lucia, C., Rinchon, A., Olmos-Alonso, A., Riecken, K., Fehse, B., Boche, D., Perry, V. H., & Gomez-Nicola, D.
- Affiliations
- University of Southampton (GB)
- University Medical Center Hamburg-Eppendorf (DE)
- ORCID
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2016-07
- Volume
- 55
- Pages
- 179-190
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC4907582
- OpenAlex
- W2119211366
- Cited by
- 110
- References
- 58
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 11 · 2023: 9 · 2022: 10 · 2021: 15 · 2020: 17 · 2019: 10 · 2018: 7 · 2017: 12 · 2016: 8
- FWCI
- 4.81
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Brain Behavior and Immunity (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (acceptedVersion)
- ORBi UMONS (submittedVersion)
- Funders
- Wessex Medical Research
- Medical Research Council (MR/K022687/1)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, hippocampal neurogenesis, chronic neurodegeneration, prion disease, CSF1R, microglial proliferation, TGF-beta, neuronal differentiation, neurogenic niche, neuroinflammation, innate immunity
- MeSH terms
- Animals, Disease Models, Animal, Hippocampus, Mice, Inbred C57BL, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor, Transforming Growth Factor beta, Prion Diseases, Microglia, Mice, Neurogenesis
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