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Alzheimer’s Disease (ad) / Micrornas / Alzheimer Disease · Journal article
Annals of Medicine · January 9, 2026
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This is a hypothesis-generating bioinformatics study combining gene expression data from PTSD and Alzheimer's disease cohorts to identify CXCL8 as a potential therapeutic target for cross-disorder neuroimmune dysregulation. Computational and preliminary experimental work suggests CXCL8 involvement in T cell recruitment and neuroinflammation, with ibuprofen proposed as a modulatory agent, but no clinical efficacy data are presented.
Integrative bioinformatics analysis combining gene expression microarray data with network pharmacology and machine learning. Human peripheral blood samples: PTSD cohort (n=109) and Alzheimer's disease cohort (n=116), each with age- and sex-matched controls. Intervention: Computational network analysis targeting CXCL8; experimental modulation with ibuprofen. Compared with: Age- and sex-matched control groups in respective datasets. Data sourced from public GEO database; study institution: Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Cross-disorder network analysis identified CXCL8 as a central hub gene linking PTSD and Alzheimer's disease pathways CXCL8 dually regulated by stress-responsive transcriptional activators and neurodegeneration-associated microRNAs Immunoassays linked CXCL8 to T cell recruitment (γδ T, CD8+ T cells)
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This work proposes CXCL8-targeted anti-inflammatory therapy as a potential dual intervention for PTSD and dementia risk mitigation. However, the absence of human clinical trial data or in vivo efficacy metrics means findings should be interpreted as hypothesis-generating and requiring validation in prospective clinical studies before informing treatment decisions.
Bioinformatics and computational analysis identifying CXCL8 as a shared molecular target in PTSD and Alzheimer's disease, with limited experimental validation and no clinical trial data.
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This work proposes CXCL8-targeted anti-inflammatory therapy as a potential dual intervention for PTSD and dementia risk mitigation. However, the absence of human clinical trial data or in vivo efficacy metrics means findings should be interpreted as hypothesis-generating and requiring validation in prospective clinical studies before informing treatment decisions.
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Background. Emerging 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.Methods. We 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.Results. Our 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+ T), suggesting its role in sustaining neuroinflammation common to both diseases. Among potential therapeutics, nonsteroidal anti-inflammatory drugs emerged as modulators of CXCL8-driven pathology, with ibuprofen significantly suppressing neurodegeneration-associated CXCL8 overexpression.Conclusions. Our 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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