Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease
Open accessAbstract
Microglia, the immune cells of the brain, can have a beneficial effect in Alzheimer's disease by phagocytosing amyloid-beta. Two-photon in vivo imaging of neuron loss in the intact brain of living Alzheimer's disease mice revealed an involvement of microglia in neuron elimination, indicated by locally increased number and migration velocity of microglia around lost neurons. Knockout of the microglial chemokine receptor Cx3cr1, which is critical in neuron-microglia communication, prevented neuron loss.
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Conflicting evidence suggests either neurotoxic or neuroprotective effects of CX3CR1 deletion in various disease models.
“Conflicting evidence in the literature suggests either neurotoxic or neuroprotective effects of CX3CR1 deletion in various disease models (Cardona et al., 2006; Fuhrmann et al., 2010).”
From CX3CR1 in Microglia Regulates Brain Amyloid Deposition through Selective Protofibrillar Amyloid-β Phagocytosis (2010) · cites this paper as Fuhrmann et al., 2010
Deletion of CX3CR1 or depression of the CX3CL1/CX3CR1 axis reduces Aβ deposition but exacerbates tau pathology, such as increased phosphorylation and aggregation of tau, and this is associated with worsened behavioral and cognitive impairments.
“Deletion of CX3CR1 or depression of the CX3CL1/CX3CR1 axis reduces Aβ deposition [130–132] but exacerbates tau pathology, such as increased phosphorylation and aggregation of tau, and this is associated with worsened behavioral and cognitive impairments [132–137] (Fig. 1).”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [134]
Housekeeping functions include synaptic remodeling, migration to sites of neuronal death for phagocytosis, and maintenance of myelin homeostasis.
“Physiological housekeeping functions include synaptic remodeling (a function critical for CNS development, homeostasis, and neurodegeneration20–22), migration to sites of neuronal death to phagocytose dead or dying cells23,24 or debris, and maintaining myelin homeostasis25.”
From Microglia in neurodegeneration (2018) · cites this paper as [23]
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- Authors
- Fuhrmann, M., Bittner, T., Jung, C. K. E., Burgold, S., Page, R. M., Mitteregger, G., Haass, C., LaFerla, F. M., Kretzschmar, H., & Herms, J.
- Affiliations
- Institut für Neuropathologie (DE)
- German Center for Neurodegenerative Diseases (DE)
- University of California, Irvine (US)
- Corresponding author
- Herms, Jochen
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2010-03-21
- Volume
- 13
- Issue
- 4
- Pages
- 411-413
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC4072212
- OpenAlex
- W2160031422
- Cited by
- 562
- References
- 15
- Citations by year
- 2026: 15 · 2025: 22 · 2024: 24 · 2023: 30 · 2022: 30 · 2021: 37 · 2020: 29 · 2019: 33 · 2018: 44 · 2017: 24 · 2016: 30 · 2015: 43 · 2014: 46 · 2013: 51 · 2012: 42
- FWCI
- 29.61
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DZNE Pub (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- Bundesministerium für Bildung und Forschung
- Bundesministerium für Wirtschaft und Technologie
- National Institute on Aging (P01AG000538)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, microglia, CX3CR1, neuronal loss, neuron-microglia communication, chemokine receptors, amyloid-beta phagocytosis, microglial migration, neurodegeneration, transgenic mouse model
- MeSH terms
- CX3C Chemokine Receptor 1, Alzheimer Disease, Animals, Cell Communication, Cell Count, Disease Models, Animal, Mice, Transgenic, Neurons, Microglia, Mice, Knockout, Receptors, Chemokine, Mice, Gene Knock-In Techniques
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