ReviewCell & bioscience2020
Interaction of Tau with the chemokine receptor, CX3CR1 and its effect on microglial activation, migration and proliferation.
Review in Cell & bioscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 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
- RNA-based therapeutics for Alzheimer's disease and related tauopathies: challenges and opportunities.The journal of prevention of Alzheimer's disease · 2026Review
- Tau-mediated Mechanisms in Alzheimer's Disease Pathogenesis.Molecular neurobiology · 2026Review
- Single nucleus RNA sequencing unveils relationship between microglia and endothelial cells in mixed Alzheimer's disease and vascular pathology.Neurobiology of disease · 2025Article
- Lipid metabolism in microglia: Emerging mechanisms and therapeutic opportunities for neurodegenerative diseases (Review).International journal of molecular medicine · 2025Review
- Targeting CX3CR1 Signaling Dynamics: A Critical Determinant in the Temporal Regulation of Post-Stroke Neurorepair.Brain sciences · 2025Review
- CX3CL1 Regulation of Gliosis in Neuroinflammatory and Neuroprotective Processes.International journal of molecular sciences · 2025Review
- Evolution of Alzheimer's Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy.Pharmaceutics · 2025Review
- CX3CR1: a potential microglia-specific PET imaging target in Alzheimer's and Parkinson's diseases.Frontiers in pharmacology · 2025Review
- Exploring the Synergistic Effects of Erinacines on Microglial Regulation and Alzheimer's Pathology Under Metabolic Stress.CNS neuroscience & therapeutics · 2024Article
- Research progress on the role of ginsenoside Rd in central nervous system diseases.African health sciences · 2024Review
- Microglial modulation as a therapeutic strategy in Alzheimer's disease: Focus on microglial preconditioning approaches.Journal of cellular and molecular medicine · 2024Review
- CX3CL1-CX3CR1 axis protects retinal ganglion cells by inhibiting microglia activation in a distal optic nerve trauma model.Inflammation and regeneration · 2024Article
- CX3CL1 (Fractalkine)-CX3CR1 Axis in Inflammation-Induced Angiogenesis and Tumorigenesis.International journal of molecular sciences · 2024Review
- Research progress in the mechanism of acupuncture regulating microglia in the treatment of Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Aging Microglia and Their Impact in the Nervous System.Advances in neurobiology · 2024Review
- Article
- Advances in proteomic phenotyping of microglia in neurodegeneration.Proteomics · 2023Review
- The innate immune response in tauopathies.European journal of immunology · 2023Review
- TGF-β1 signalling in Alzheimer's pathology and cytoskeletal reorganization: a specialized Tau perspective.Journal of neuroinflammation · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease that leads to progressive loss of memory and dementia. The pathological hallmarks of AD include extracellular accumulation of amyloid-β peptides forming senile plaques and intracellular accumulation of Tau oligomers and filamentous species. Tau is a microtubule-binding protein that stabilizes tubulin to form microtubules under physiological condition. In AD/ pathological condition, Tau detaches from microtubules and aggregates to form oligomers of different sizes and filamentous species such as paired helical filaments. Microglia are the resident brain macrophages that are involved in the phagocytosis of microbes, cellular debris, misfolded and aggregated proteins. Chemokine receptor, CX3CR1 is mostly expressed on microglia and is involved in maintaining the microglia in a quiescent state by binding to its ligand, fractalkine (CX3CL1), which is expressed in neurons as both soluble or membrane-bound state. Hence, under physiological conditions, the CX3CR1/CX3CL1 axis plays a significant role in maintaining the central nervous system (CNS) homeostasis. Further, CX3CR1/CX3CL1 signalling is involved in the synthesis of anti-inflammatory cytokines and also has a significant role in cytoskeletal rearrangement, migration, apoptosis and proliferation. In AD brain, the expression level of fractalkine is reduced, and hence Tau competes to interact with its receptor, CX3CR1. In microglia, phagocytosis and internalization of extracellular Tau species occurs in the presence of a chemokine receptor, CX3CR1 which binds directly to Tau and promotes its internalization. In this review, the pathophysiological roles of CX3CR1/fractalkine signalling in microglia and neurons at different stages of Alzheimer's disease and the possible role of CX3CR1/Tau signalling has been widely discussed.
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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.