Neuronal Cx3cr1 Deficiency Protects against Amyloid β-Induced Neurotoxicity
Open accessAbstract
Cx3cr1, the receptor for the chemokine Cx3cl1 (fractalkine), has been implicated in the progression and severity of Alzheimer's disease-like pathology in mice, but the underlying mechanisms remain unclear. A complicating factor is that Cx3cr1 has been demonstrated in both neurons and microglia. Here, we have dissected the differences between neuronal and microglial Cx3cr1, specifically by comparing direct amyloid-β-induced toxicity in cultured, mature, microglia-depleted hippocampal neurons from wild-type and Cx3cr1-/- mice. Wild-type neurons expressed both Cx3cl1 and Cx3cr1 and released Cx3cl1 in response to amyloid-β. Knockout of neuronal Cx3cr1 abated amyloid-β-induced lactate dehydrogenase release. Furthermore, amyloid-β differentially induced depression of pre- and postsynaptic components of miniature excitatory postsynaptic currents, in a peptide conformation-dependent manner. Knockout of neuronal Cx3cr1 abated effects of both amyloid-β conformational states, which were differentiable by aggregation kinetics and peptide morphology. We obtained similar results after both acute and chronic treatment of cultured neurons with the Cx3cr1 antagonist F1. Thus, neuronal Cx3cr1 may impact Alzheimer's disease-like pathology by modulating conformational state-dependent amyloid-β-induced synaptotoxicity.
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The hippocampus is thought to be particularly vulnerable to insults.
“it is thought to be particularly vulnerable to insults17.”
From Constitutive expression of CX3CR1-BAC-Cre introduces minimal off-target effects in microglia (2026) · cites this paper as [17]
The Discussion says hippocampal neurons are more susceptible than cortical neurons to Aβ toxicity. That supports particular vulnerability to one insult, but the claim generalizes to insults more broadly, which this passage does not establish. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe hippocampus recapitulates the developmental trajectory throughout life.
“Since the hippocampus recapitulates the developmental trajectory throughout life”
From Constitutive expression of CX3CR1-BAC-Cre introduces minimal off-target effects in microglia (2026) · cites this paper as [17]
The Results describe Cx3cr1 expression in cultured postnatal mouse hippocampal neurons, not the hippocampus’s developmental trajectory throughout life. The Discussion notes that the study’s neonatal, in vitro model limits its application to the aging human CNS. Searches for the claimed trajectory and adult hippocampal neurogenesis found no passage addressing the claim. (LLM, conf=0.76)
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Septyaningtrias, D. E., Sholikah, T. A., Suhda, S., Sumiwi, Y. A. A., & Susilowati, R. (2025) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-025-10245-y · Cited by 2 · see citing works
Impaired Signaling of NF-κB and NRF2 in CX3CR1-Deficient Microglia: Implications in TauopathiesPreprint
Castro‐Sánchez, S., García‐Yagüe, Á. J., Kügler, S., & Lastres‐Becker, I. (2018) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/346304 · Cited by 2 · see citing works
Ananathanarayana, V., Upadhyay, R., Illanad, G. H., Krishnan, D., Bochageri, N. P., Sevanan, M., Bagewadi, Z., Sivasamy, R., & Chinnathambi, S. (2025) · Advances in immunology · doi:10.1016/bs.ai.2025.11.002
- Authors
- Dworzak, J., Renvoisé, B., Habchi, J., Yates, E. V., Combadière, C., Knowles, T. P., Dobson, C. M., Blackstone, C., Paulsen, O., & Murphy, P. M.
- Affiliations
- National Institutes of Health (US)
- University of Cambridge (GB)
- Inserm (FR)
- Corresponding author
- Paulsen, Ole
- Murphy, Philip M.
- ORCID
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-06-03
- Volume
- 10
- Issue
- 6
- Pages
- e0127730
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4454597
- OpenAlex
- W576141130
- Cited by
- 30
- References
- 57
- Citations by year
- 2026: 1 · 2025: 3 · 2023: 5 · 2022: 6 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 5 · 2016: 5
- FWCI
- 2.46
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- public-domain
- creativecommons.org/publicdomain/zero/1.0/ (vor)
- Locations
- PLoS ONE (publishedVersion, public-domain)
- PubMed Central (publishedVersion, public-domain)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases
- National Institute of Neurological Disorders and Stroke
- NHLBI Division of Intramural Research
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- CX3CR1, fractalkine, amyloid-beta, Alzheimer's disease, microglia, synaptotoxicity, excitatory postsynaptic currents, peptide aggregation, hippocampal neurons, neuroprotection
- MeSH terms
- CX3C Chemokine Receptor 1, Alzheimer Disease, Animals, Disease Models, Animal, Synaptic Transmission, Neurons, Amyloid beta-Peptides, Mice, Knockout, Receptors, Chemokine, Mice, Protein Aggregation, Pathological
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