ArticlePloS one2015
Neuronal Cx3cr1 Deficiency Protects against Amyloid β-Induced Neurotoxicity.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Blood and CSF chemokines in Alzheimer's disease and mild cognitive impairment: a systematic review and meta-analysis.Alzheimer's research & therapy · 2023Pooled it
- TNF-α Inhibition Modulates CX3CR1, Pyroptosis-related Genes, and BDNF to Alleviate Anxiety-like Behavior in Type 2 Diabetic Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- CX3CL1 Regulation of Gliosis in Neuroinflammatory and Neuroprotective Processes.International journal of molecular sciences · 2025Review
- CX3CL1 Pathway as a Molecular Target for Treatment Strategies in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Age-dependent changes on fractalkine forms and their contribution to neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- Fractalkine/CX3CR1-Dependent Modulation of Synaptic and Network Plasticity in Health and Disease.Neural plasticity · 2023Review
- Role of Chemokines in the Development and Progression of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- Crosstalk between Microglia and Neurons in Neurotrauma: An Overview of the Underlying Mechanisms.Current neuropharmacology · 2022Review
- Integrative analysis of DNA methylation and gene expression identifies genes associated with biological aging in Alzheimer's disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- Physical Exercise-Induced Myokines in Neurodegenerative Diseases.International journal of molecular sciences · 2021Review
- Tissue-specific Role of CXImmune network · 2018Review
- Ischemia-induced Neuronal Cell Death Is Mediated by Chemokine Receptor CX3CR1.Scientific reports · 2018Article
- Bidirectional Microglia-Neuron Communication in Health and Disease.Frontiers in cellular neuroscience · 2018Review
- Pharmacological Tools to Activate Microglia and their Possible use to Study Neural Network Patho-physiology.Current neuropharmacology · 2017Review
- Progesterone Attenuates Microglial-Driven Retinal Degeneration and Stimulates Protective Fractalkine-CX3CR1 Signaling.PloS one · 2016Article
- CX3CL1/CX3CR1 in Alzheimer's Disease: A Target for Neuroprotection.BioMed research international · 2016Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
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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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.