ArticleThe Journal of clinical investigation2015
CXCR3 promotes plaque formation and behavioral deficits in an Alzheimer's disease model.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses 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.
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Who cites it
89 citing papers in PubMed, 2 syntheses or guidelines pooled it, 144 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
- Chemokines in patients with Alzheimer's disease: A meta-analysis.Frontiers in aging neuroscience · 2023Pooled it
- Canonical lymphocyte chemokine receptors CXCR3 and CXCR5 modulate neuronal autophagy.Cell death and differentiation · 2026Article
- Oxyberberine-nanoparticle attenuates the cognitive deficits in a transgenic mouse model of Alzheimer's disease via modulating gut microbiota through suppressing CXCL10/CXCR3 pathway.Acta pharmacologica Sinica · 2026Article
- Chemokines in Alzheimer's Disease: Early Defence, Late Damage and the Impact of Sex and Infection.Basic & clinical pharmacology & toxicology · 2026Review
- Microglial mitophagy as an immunometabolic checkpoint in alzheimer's disease: linking mitochondrial quality control to neuroinflammation.Journal of neuroinflammation · 2026Review
- The Immune-Chemokine Axis in Alzheimer's Disease: Roles of Adaptive Immune System in Neuroinflammation and Disease Progression.Biomolecules · 2026Review
- Type I interferon drives T cell responses to amyloid beta in the central nervous system.Nature communications · 2026Article
- Melanoma cell inoculation improves cognitive impairment in the 5xFAD mouse model of Alzheimer's disease.Scientific reports · 2026Article
- Autoimmune signatures in neurodegenerative dementias: from peripheral immune activation to CNS pathology.Frontiers in immunology · 2026Review
- Peripheral immune profiling in frontotemporal dementia.Brain communications · 2026Article
- CXCR3 Deficiency Alleviates Retinal Ganglion Cell Loss by Regulating Neuron-Astrocyte Communication in a Mouse Model of Glaucoma.Investigative ophthalmology & visual science · 2025Article
- C‑X‑C Motif Chemokine 10/C-X‑C Motif Chemokine Receptor 3 Signaling Induces Neural Senescence and Cognitive Impairments.ACS pharmacology & translational science · 2025Article
- Hippocampal CA1 neuron, a crucial regulator for chronic stress exacerbating Alzheimer's disease progression.Cell & bioscience · 2025Article
- Serotonergic Regulation in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Balancing Microglial Density and Activation in Central Nervous System Development and Disease.Current issues in molecular biology · 2025Review
- CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson's disease models.Journal of neuroinflammation · 2025Article
- NEK7 induces lactylation in Alzheimer's disease to promote pyroptosis in BV-2 cells.Molecular brain · 2024Article
- Animal models of Alzheimer's disease: Current strategies and new directions.Zoological research · 2024Review
- Early blood immune molecular alterations in cynomolgus monkeys with a PSEN1 mutation causing familial Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemokines are important modulators of neuroinflammation and neurodegeneration. In the brains of Alzheimer's disease (AD) patients and in AD animal models, the chemokine CXCL10 is found in high concentrations, suggesting a pathogenic role for this chemokine and its receptor, CXCR3. Recent studies aimed at addressing the role of CXCR3 in neurological diseases indicate potent, but diverse, functions for CXCR3. Here, we examined the impact of CXCR3 in the amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mouse model of AD. We found that, compared with control APP/PSI animals, plaque burden and Aβ levels were strongly reduced in CXCR3-deficient APP/PS1 mice. Analysis of microglial phagocytosis in vitro and in vivo demonstrated that CXCR3 deficiency increased the microglial uptake of Aβ. Application of a CXCR3 antagonist increased microglial Aβ phagocytosis, which was associated with reduced TNF-α secretion. Moreover, in CXCR3-deficient APP/PS1 mice, microglia exhibited morphological activation and reduced plaque association, and brain tissue from APP/PS1 animals lacking CXCR3 had reduced concentrations of proinflammatory cytokines compared with controls. Further, loss of CXCR3 attenuated the behavioral deficits observed in APP/PS1 mice. Together, our data indicate that CXCR3 signaling mediates development of AD-like pathology in APP/PS1 mice and suggest that CXCR3 has potential as a therapeutic target for AD.
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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.