ArticleThe Journal of experimental medicine2019
The intracellular domain of CX3CL1 regulates adult neurogenesis and Alzheimer's amyloid pathology.
Article in The Journal of experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Matrix metalloproteinase-9 is associated with CX3CL1 on tau and amyloid biomarker pathways in APOE4 carriers.Neurobiology of disease · 2026Trial
- The neuroimmune system and cognition.Nature immunology · 2026Review
- Advances in the multifunctional roles of CX3CL1 in the central nervous system.Frontiers in aging neuroscience · 2026Review
- Targeting microglia-mediated neuroinflammation in Alzheimer's disease: mechanisms and therapeutic approaches.Frontiers in immunology · 2026Review
- Formulation and Evaluation of Astaxanthin-Loaded Invasomes as Therapeutic Approaches for Alzheimer's Disease Induced in Rats: Role of SIRT-1/BDNF/miRNA-134/GSK-3β Signaling.Molecular neurobiology · 2025Article
- SARS-CoV-2 vaccination during pregnancy enhances offspring hippocampal neurogenesis and working memory via IFN-γ-responsive microglia.Communications biology · 2025Article
- CX3CL1 Regulation of Gliosis in Neuroinflammatory and Neuroprotective Processes.International journal of molecular sciences · 2025Review
- Treadmill Exercise Enhances Post-Stroke Functional Recovery in Mice via the CX3CL1/CX3CR1 Signaling Pathway.Molecular neurobiology · 2025Article
- Expression of CX3CL1 in the neoplastic lung tissue of squamous cell lung cancer.Journal of Cancer · 2025Article
- Physical Exercise Counteracts Aging-Associated White Matter Demyelination Causing Cognitive Decline.Aging and disease · 2024Review
- Fractalkine in Health and Disease.International journal of molecular sciences · 2024Review
- Fractalkine isoforms differentially regulate microglia-mediated inflammation and enhance visual function in the diabetic retina.Journal of neuroinflammation · 2024Article
- Therapeutic Delivery of Soluble Fractalkine Ameliorates Vascular Dysfunction in the Diabetic Retina.International journal of molecular sciences · 2024Article
- CX3CL1/CX3CR1 Signaling Mediated Neuroglia Activation Is Implicated in the Retinal Degeneration: A Potential Therapeutic Target to Prevent Photoreceptor Death.Investigative ophthalmology & visual science · 2024Article
- Exploration of C-terminal CX3CL1 for reducing age-dependent neurodegeneration.Neural regeneration research · 2023Article
- Spinal Cord Stimulation Increases Chemoefficacy and Prevents Paclitaxel-Induced Pain via CX3CL1.Neuromodulation : journal of the International Neuromodulation Society · 2023Article
- CX3CL1 Pathway as a Molecular Target for Treatment Strategies in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- The Cytokine CX3CL1 and ADAMs/MMPs in Concerted Cross-Talk Influencing Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Article
- Age-dependent changes on fractalkine forms and their contribution to neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The membrane-anchored CX3CL1 is best known to exert its signaling function through binding its receptor CX3CR1. This study demonstrates a novel function that CX3CL1 exerts. CX3CL1 is sequentially cleaved by α-, β-, and γ-secretase, and the released CX3CL1 intracellular domain (CX3CL1-ICD) would translocate into the cell nucleus to alter gene expression due to this back-signaling function. Amyloid deposition and neuronal loss were significantly reduced when membrane-anchored CX3CL1 C-terminal fragment (CX3CL1-ct) was overexpressed in Alzheimer's 5xFAD mouse model. The reversal of neuronal loss in 5xFAD can be attributed to increased neurogenesis by CX3CL1-ICD, as revealed by morphological and unbiased RNA-sequencing analyses. Mechanistically, this CX3CL1 back-signal likely enhances developmental and adult neurogenesis through the TGFβ2/3-Smad2/3 pathway and other genes important for neurogenesis. Induction of CX3CL1 back-signaling may not only be a promising novel mechanism to replenish neuronal loss but also for reducing amyloid deposition for Alzheimer's treatment.
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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.