Publication date: Dec 09, 2025
Atrazine (ATZ), a widely used herbicide, is implicated in neurodegenerative risks, yet its neurotoxic mechanisms remain unclear. This study investigates how environmentally relevant ATZ exposure disrupts neuron-microglia interactions to drive Parkinson’s disease (PD)-like pathology. C57BL/6 mice received 28-day oral ATZ (10 mg/kg/day). Behavioral phenotyping (open field, pole climb, wire hanging tests) assessed motor deficits. Midbrain tissues underwent histopathology and single-cell RNA sequencing (scRNA-seq). Intercellular communication networks were reconstructed using the CellChat algorithm, with a focus on neuron-microglia signaling pathways. Quantitative real-time PCR (qPCR) was employed to validate the transcriptomic accuracy of scRNA-seq (n = 6/group). ATZ induced PD-like motor dysfunction (e. g., mean speed in OFT, P
| Concepts | Keywords |
|---|---|
| 10mg | Atrazine |
| Herbicide | Crosstalk between cells |
| Mice | Microglia |
| Parkinson | Parkinson’s disease |
| Transcriptomics | Single-cell transcriptomics |
Semantics
| Type | Source | Name |
|---|---|---|
| disease | MESH | Parkinson’s disease |
| drug | DRUGBANK | Atazanavir |