ReviewJournal of neuropathology and experimental neurology2023
The intricate role of CCL5/CCR5 axis in Alzheimer disease.
Review in Journal of neuropathology and experimental neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 28 citations in OpenAlex.
- Microglial HDAC3 inhibits the migration of CD8-positive T cell in the development of EAE by restraining the expression of CCL5.Cell & bioscience · 2026Article
- Chemokine Networks in Blood-Brain Barrier Regulation: Bidirectional Mechanisms, Clinical Translation, and Precision Therapeutic Prospects.Biomolecules · 2026Review
- Postoperative neurocognitive disorder: migration and crosstalk of inflammation in the peripheral and central nervous system.Perioperative medicine (London, England) · 2026Review
- Astrocytic CCL5 orchestrates CCR5-positive neuronal necroptosis in subarachnoid hemorrhage.Journal of neuroinflammation · 2026Article
- Mechanisms of transcriptional regulation of CCR5, which is the co-receptor for R5-tropic HIV and is also involved in other disease processes.Biochemical Society transactions · 2026Review
- More than Dysbiosis: Imbalance in Humoral and Neuronal Bidirectional Crosstalk Between Gut and Brain in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Cryptococcus exploits delayed microglial activation, and microglial osteopontin/Spp1 impairs peripheral host control.Cell host & microbe · 2025Article
- GPR75: Advances, Challenges in Deorphanization, and Potential as a Novel Drug Target for Disease Treatment.International journal of molecular sciences · 2025Review
- Novel full-thickness biomimetic corneal model for studying pathogenesis and treatment of diabetic keratopathy.Materials today. Bio · 2025Article
- Inflammatory biomarkers profiles and cognition among older adults.Scientific reports · 2025Article
- Curcumin-piperine nanoparticles mitigate cuprizone-induced cognitive impairment via antioxidant and anti-inflammatory mechanisms.Frontiers in nutrition · 2025Article
- Mechanically-adaptive, resveratrol-eluting neural probes for improved intracortical recording performance and stability.Npj flexible electronics · 2025Article
- An exploratory analysis of bezisterim treatment associated with decreased biological age acceleration, and improved clinical measure and biomarker changes in mild-to-moderate probable Alzheimer's disease.Frontiers in neuroscience · 2025Article
- The contributing role of CCR5 in dementia.Frontiers in neurology · 2025Review
- Repurposing lapatinib as a triple antagonist of chemokine receptors 3, 4, and 5.Molecular pharmacology · 2025Article
- Transcriptome analysis of the aged SAMP8 mouse model of Alzheimer's disease reveals novel molecular targets of formononetin protection.Frontiers in pharmacology · 2024Article
- Spotlight on pro-inflammatory chemokines: regulators of cellular communication in cognitive impairment.Frontiers in immunology · 2024Review
- Targeting the chemokine-microglia nexus: A novel strategy for modulating neuroinflammation in Alzheimer's disease.Journal of Alzheimer's disease reportsReview
- Clinical outcomes and anti-inflammatory mechanisms of nucleus basalis of Meynert deep brain stimulation in Alzheimer's disease.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The morbidity and mortality associated with Alzheimer disease (AD), one of the most common neurodegenerative diseases, are increasing each year. Although both amyloid β and tau proteins are known to be involved in AD pathology, their detailed functions in the pathogenesis of the disease are not fully understood. There is increasing evidence that neuroinflammation contributes to the development and progression of AD, with astrocytes, microglia, and the cytokines and chemokines they secrete acting coordinately in these processes. Signaling involving chemokine (C-C motif) ligand 5 (CCL5) and its main receptor C-C chemokine receptor 5 (CCR5) plays an important role in normal physiologic processes as well as pathologic conditions such as neurodegeneration. In recent years, many studies have shown that the CCL5/CCR5 axis plays a major effect in the pathogenesis of AD, but there are also a few studies that contradict this. In short, the role of CCL5/CCR5 axis in the pathogenesis of AD is still intricate. This review summarizes the structure, distribution, physiologic functions of the CCL5/CCR5 axis, and the progress in understanding its involvement in the pathogenesis of AD.
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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.