ArticleAnnals of medicine2026
Targeting CXCL8 in post-traumatic stress disorder and Alzheimer's disease: insights from cross-disorder molecular analysis.
Article in Annals of medicine, 2026. 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
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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
1 citing paper in PubMed.
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEmerging clinical evidence indicates that post-traumatic stress disorder (PTSD) may accelerate Alzheimer's disease progression, yet the molecular mechanisms linking these disorders remain poorly understood.
methodsWe conducted an integrative bioinformatics analysis combining blood cell profiles from PTSD and Alzheimer's disease cohorts to identify shared pathogenic pathways and therapeutic targets. Computational drug repositioning and experimental validation were used to pinpoint effective treatments.
resultsOur analysis revealed convergent dysregulation in neuroimmune and metabolic pathways, including compensatory upregulation of terpenoid biosynthesis and impaired JAK-STAT neuroprotective signaling. Cross-disorder network analysis identified CXCL8 as a central hub gene, prioritized through network pharmacology and machine learning. Mechanistic studies demonstrated that CXCL8 is dually regulated by stress-responsive transcriptional activators and neurodegeneration-associated microRNAs, positioning it as a key mediator of peripheral-central immune crosstalk. Immunoassays further linked CXCL8 to T cell recruitment (γδ T, CD8
conclusionsOur findings highlight CXCL8-mediated neuroimmune dysregulation as a critical link between PTSD and Alzheimer's disease, supporting targeted anti-inflammatory strategies to mitigate stress-related dementia risk. This study advances a precision medicine framework for neurodegenerative comorbidities by integrating cross-disease molecular signatures.
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