ArticleJournal of clinical medicine2022
High Cerebrospinal Fluid CX3CL1 Levels in Alzheimer's Disease Patients but Not in Non-Alzheimer's Disease Dementia.
Article in Journal of clinical medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- The glia-immune network: Astrocytes and oligodendrocytes as microglial co-ordinators in health and disease.The Journal of physiology · 2026Review
- Advances in the multifunctional roles of CX3CL1 in the central nervous system.Frontiers in aging neuroscience · 2026Review
- Article
- Insights into Biomarkers of Alzheimer's Disease: From Core Markers to Emerging Directions.Aging and disease · 2025Review
- CX3CL1 Regulation of Gliosis in Neuroinflammatory and Neuroprotective Processes.International journal of molecular sciences · 2025Review
- Diagnostic potential of urinary CX3CL1 for amnestic mild cognitive impairment and Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Nucleic Acids-Based Biomarkers for Alzheimer's Disease Diagnosis and Novel Molecules to Treat the Disease.International journal of molecular sciences · 2024Review
- Effects of Cerebrospinal Fluids from Alzheimer and Non-Alzheimer Patients on Neurons-Astrocytes-Microglia Co-Culture.International journal of molecular sciences · 2024Article
- More than microglia: myeloid cells and biomarkers in neurodegeneration.Frontiers in neuroscience · 2024Review
- Cerebrospinal and Blood Biomarkers in Alzheimer's Disease: Did Mild Cognitive Impairment Definition Affect Their Clinical Usefulness?International journal of molecular sciences · 2023Review
- Mechanism Exploration of Amyloid-β-42 Disaggregation by Single-Chain Variable Fragments of Alzheimer's Disease Therapeutic Antibodies.International journal of molecular sciences · 2023Article
- CX3CL1 Pathway as a Molecular Target for Treatment Strategies in Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Pharmacological Inhibition of the Asparaginyl Endopeptidase (AEP) in an Alzheimer's Disease Model Improves the Survival and Efficacy of Transplanted Neural Stem Cells.International journal of molecular sciences · 2023Article
- Recovery of Bioactive Compounds from Marine Organisms: Focus on the Future Perspectives for Pharmacological, Biomedical and Regenerative Medicine Applications of Marine Collagen.Molecules (Basel, Switzerland) · 2023Review
- Microglial Activation and Priming in Alzheimer's Disease: State of the Art and Future Perspectives.International journal of molecular sciences · 2023Review
- BACE1 Inhibitors for Alzheimer's Disease: The Past, Present and Any Future?Molecules (Basel, Switzerland) · 2022Review
- The Common Alzheimer's Disease Research Ontology (CADRO) for biomarker categorization.Alzheimer's & dementia (New York, N. Y.)Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common form of cognitive decline worldwide, occurring in about 10% of people older than 65 years. The well-known hallmarks of AD are extracellular aggregates of amyloid β (Aβ) and intracellular neurofibrillary tangles (NFTs) of tau protein. The evidence that Aβ overproduction leads to AD has paved the way for the AD pathogenesis amyloid cascade hypothesis, which proposes that the neuronal damage is sustained by Aβ overproduction. Consistently, AD cerebrospinal fluid (CSF) biomarkers used in clinical practice, including Aβ 1-42, Aβ 1-40, Aβ 42/40 ratio, and pTau, are related to the amyloid hypothesis. Recently, it was suggested that the Aβ deposition cascade cannot fully disclose AD pathogenesis, with other putative players being involved in the pathophysiology of the disease. Among all, one of the most studied factors is inflammation in the brain. Hence, biomarkers of inflammation and microglia activation have also been proposed to identify AD. Among them, CX3 chemokine ligand 1 (CX3CL1) has taken center stage. This transmembrane protein, also known as fractalkine (FKN), is normally expressed in neurons, featuring an N-terminal chemokine domain and an extended mucin-like stalk, following a short intra-cytoplasmatic domain. The molecule exists in both membrane-bound and soluble forms. It is accepted that the soluble and membrane-bound forms of FKN evoke differential signaling within the CNS. Given the link between CX3XL1 and microglial activation, it has been suggested that CX3CL1 signaling disruption could play a part in the pathogenesis of AD. Furthermore, a role for chemokine as a biomarker has been proposed. However, the findings collected are controversial. The current study aimed to describe the cerebrospinal fluid (CSF) levels of CX3XL1 and classical biomarkers in AD patients.
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