ArticleBMC geriatrics2025
LAX1 as a core biomarker in Alzheimer's disease and periodontitis via the STAT signaling pathway.
Article in BMC geriatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- STAT6-Mediated SOCS2 Alleviates Cognitive Impairments and Neuronal Damage in Alzheimer's Disease Rat Models and Aβ1-42-Stimulated HT-22 Cells.Molecular neurobiology · 2026Article
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.
Funding
Abstract
backgroundThe relationship between Alzheimer's disease (AD) and chronic periodontitis (PD) rarely share the medical spotlight, yet epidemiological mirroring hints at a common inflammatory root.
methodsMining four GEO (Gene Expression Omnibus) cohorts (211 AD + 27 controls; 24 PD + 23 controls), batch-corrected and validated by principal component analysis (PCA)/t-distributed stochastic neighbour embedding (t-SNE)/uniform manifold approximation and projection (UMAP), we identified 61 shared differentially expressed genes (DEGs) with lymphocyte transmembrane adaptor 1 (LAX1) ranked first in weighted gene co-expression network analysis (WGCNA), maximum clique centrality (MCC), Degree, edge percolated component (EPC) and Stress algorithms, tightly co-expressed with colony-stimulating factor 3 receptor (CSF3R) and signal transducer and activator of transcription 1/3 (STAT1/3). Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene set enrichment analysis (GSEA) uniquely highlighted the "LAX1/CSF3R/STAT" triad in apoptosis and JAK-STAT cascades. CIBERSORT de-convolution showed LAX1 covaried with plasma-cell, mast-cell and M0-macrophage infiltration.
resultsPlasma from 42 AD and 38 stage-III/IV PD patients showed elevated soluble LAX1 (sLAX1) correlating with Mini-Mental State Examination (MMSE) decline (r =-0.67) and clinical attachment loss (r = 0.71), outperforming Aβ42 and receptor activator of nuclear factor-κB ligand (RANKL) in receiver operating characteristic (ROC) analyses (area under the curve [AUC] = 0.91). We hypothesised that LAX1 orchestrates the dialogue via the STAT axis. In human periodontal-ligament fibroblasts and 5 × FAD glia exposed to Porphyromonas gingivalis LPS or amyloid-β42 (Aβ42), LAX1 overexpression (pCMV6-LAX1) amplified STAT1/3 phosphorylation, elevated interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) by 2.3-3.1-fold and escalated p53, cleaved caspase-3 and FAS, whereas LAX1 small interfering RNA (siRNA) abolished these effects. In other words, targeting of the LAX1 validated that the inflammatory/apoptotic signature scales with LAX1 abundance.
conclusionLAX1 gates STAT-dependent neuroinflammation and periodontal destruction, offering a druggable checkpoint and blood-based biomarker for these convergent chronic diseases.
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.