CCR5 as a Key Mediator: Insights into the Molecular Mechanisms by Which Air Pollutants Induce Alzheimer's Disease via Network Toxicology and Molecular Docking - PubMed
4 hours ago
- #Molecular Docking
- #Alzheimer's Disease
- #Air Pollution
- The study combined network toxicology and molecular docking to investigate how seven air pollutants (benzene, toluene, O3, SO2, NO, NO2, CO) contribute to Alzheimer's disease (AD).
- Researchers identified 88 overlapping genes from pollutant-related and AD-related targets, with enrichment analyses linking them to neuronal apoptosis, inflammatory responses, MAPK, and PI3K-Akt signaling pathways.
- External validation pinpointed CCR5, PLD3, CCL2, and RET as core targets, with CCR5 showing the highest diagnostic efficacy (AUC = 0.85) for AD.
- Molecular docking simulations revealed that all seven pollutants could spontaneously bind to core proteins, with benzene and toluene exhibiting the strongest and most stable interactions with CCR5 (binding energy < -5kcal/mol).
- The findings suggest CCR5 as a key molecular mediator in the link between air pollution and AD, providing a novel mechanistic perspective and supporting CCR5-targeted preventive or therapeutic strategies.