ArticleThe international journal of neuropsychopharmacology2024
Investigating the Impact of IL-6 and CXCL8 on Neurodegeneration and Cognitive Decline in Alzheimer Disease.
Article in The international journal of neuropsychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting CXCL8 in post-traumatic stress disorder and Alzheimer's disease: insights from cross-disorder molecular analysis.Annals of medicine · 2026Article
- Causality relationship between 91 inflammatory factors and Alzheimer disease: A bidirectional Mendelian randomization study.Medicine · 2026Article
- ATM interaction with GRP94 modulates oncogenic receptor expression and signaling and microglial activation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Endothelin-1 triggers oxidative stress and cytokine release in human microglia cells through ETRB-dependent mechanisms.Frontiers in cellular neuroscience · 2025Article
- Network Pharmacology of miR-146a-5p as a Potential Anti-Inflammatory Agent in Preventing Alzheimer's Disease.Current Alzheimer research · 2025Article
- N-Glycosylation and Alzheimer's disease: A 2001-2025 global bibliometric landscape revealing emerging diagnostic trends.Journal of Alzheimer's disease reportsArticle
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
backgroundAlzheimer disease (AD) is a progressive neurodegenerative disorder primarily affecting the elderly, characterized by severe cognitive impairment and memory loss. Emerging evidence suggests that neuroinflammation plays a significant role in AD pathogenesis, with cytokines like interleukin-6 (IL-6) and C-X-C motif chemokine ligand 8 (CXCL8) contributing to the disease progression.
methodsWe utilized Gene Expression Omnibus datasets to identify IL-6 and CXCL8 as pivotal inflammatory markers in AD. In vitro experiments were conducted using SK-N-BE(2)-M17 and THP-1 cell lines treated with IL-6 and CXCL8 to model AD. Additionally, in vivo tests on Amyloid Precursor Protein/Presenilin 1 (APP/PS1) AD mouse models were performed to assess the impact of these cytokines on cognitive functions and brain pathology.
resultsThe results indicated a significant decrease in cell viability, increased apoptosis, and elevated inflammatory factor secretion following IL-6 and CXCL8 treatment in vitro. In vivo, AD mouse models treated with these cytokines exhibited exacerbated emotional distress, decreased social interaction, impaired cognitive functions, and increased amyloid protein deposition in neural tissues.
conclusionsThe study highlights the detrimental effects of IL-6 and CXCL8 on neuronal health and cognitive functions in AD. These findings suggest that targeting these cytokines could offer potential therapeutic interventions for improving patient outcomes in Alzheimer disease.
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