ArticleAlzheimer's research & therapy2023
Convergent transcriptomic and genomic evidence supporting a dysregulation of CXCL16 and CCL5 in Alzheimer's disease.
Article in Alzheimer's research & therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Chemokines in patients with Alzheimer's disease: A meta-analysis.Frontiers in aging neuroscience · 2023Pooled it
- Chemokines in Alzheimer's Disease: Early Defence, Late Damage and the Impact of Sex and Infection.Basic & clinical pharmacology & toxicology · 2026Review
- Cell-to-cell variability and gain of methylation at polycomb CpG islands as a hallmark of aging.Nature communications · 2026Article
- Ginsenoside Rg1 Ameliorates the Learning and Memory Deficits of 5xFAD Mice by Inhibiting CCR3 Activity: Insights from In Vivo and In Vitro Investigations.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Sex specific effects of a high fat diet on metabolism, cognition, and pathology in the Tg-SwDI mouse model of Alzheimer's disease.Journal of neuroinflammation · 2026Article
- Cystathionine γ-lyase is a major regulator of cognitive function through neurotrophin signaling and neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A multivariate approach to identify association between peripheral blood DNA methylation and cerebrospinal fluid biomarkers of Alzheimer disease.Scientific reports · 2025Article
- The involvement of microglia and the CXCL16-CXCR6 axis in the recruitment of CD8Scientific reports · 2025Article
- Microglial deficiency in the ATRX chromatin remodeler elicits a viral mimicry immune response that impacts neuronal function and behavior.PLoS biology · 2025Article
- Multi-Omics Analysis of Hippocampus in Rats Administered Trimethyltin Chloride.Neurotoxicity research · 2025Article
- Molecular pathogenesis of Alzheimer's disease onset in a mouse model: effects of cannabidiol treatment.Frontiers in neuroscience · 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
- Large-scale deep proteomic analysis in Alzheimer's disease brain regions across race and ethnicity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Silencing CXCL16 alleviate neuroinflammation and M1 microglial polarization in mouse brain hemorrhage model and BV2 cell model through PI3K/AKT pathway.Experimental brain research · 2024Article
- Article
- Switch of innate to adaptative immune responses in the brain of patients with Alzheimer's disease correlates with tauopathy progression.npj aging · 2024Article
- Review
- Inflammation, Autoimmunity and Neurodegenerative Diseases, Therapeutics and Beyond.Current neuropharmacology · 2024Article
- Targeting the chemokine-microglia nexus: A novel strategy for modulating neuroinflammation in Alzheimer's disease.Journal of Alzheimer's disease reportsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuroinflammatory factors, especially chemokines, have been widely reported to be involved in the pathogenesis of Alzheimer's disease (AD). It is unclear how chemokines are altered in AD, and whether dysregulation of chemokines is the cause, or the consequence, of the disease.
methodsWe initially screened the transcriptomic profiles of chemokines from publicly available datasets of brain tissues of AD patients and mouse models. Expression alteration of chemokines in the blood from AD patients was also measured to explore whether any chemokine might be used as a potential biomarker for AD. We further analyzed the association between the coding variants of chemokine genes and genetic susceptibility of AD by targeted sequencing of a Han Chinese case-control cohort. Mendelian randomization (MR) was performed to infer the causal association of chemokine dysregulation with AD development.
resultsThree chemokine genes (CCL5, CXCL1, and CXCL16) were consistently upregulated in brain tissues from AD patients and the mouse models and were positively correlated with Aβ and tau pathology in AD mice. Peripheral blood mRNA expression of CXCL16 was upregulated in mild cognitive impairment (MCI) and AD patients, indicating the potential of CXCL16 as a biomarker for AD development. None of the coding variants within any chemokine gene conferred a genetic risk to AD. MR analysis confirmed a causal role of CCL5 dysregulation in AD mediated by trans-regulatory variants.
conclusionsIn summary, we have provided transcriptomic and genomic evidence supporting an active role of dysregulated CXCL16 and CCL5 during AD development.
Indexed as
Identifiers
What OpenQuestion holds
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.