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Neurotoxic mechanisms of microplastic compounds in Alzheimer's and Parkinson's diseases: A network toxicology and molecular docking study
Original title: "Neurotoxic mechanisms of microplastic compounds in Alzheimer’s and Parkinson’s diseases: A network toxicology and molecular docking study"
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Scientists used computer modeling to study how tiny plastic particles from our environment might affect brain proteins linked to Alzheimer's and Parkinson's diseases. They found that certain microplastic compounds can cross the blood-brain barrier and strongly interact with proteins involved in nerve cell death and brain signaling, suggesting a possible link between plastic pollution exposure and these neurodegenerative diseases. This is early-stage computational research, not a study in living humans, but it points to a concerning connection that deserves more investigation and stronger regulation of microplastics.
Microplastic compounds (MPCs), pervasive environmental pollutants, are increasingly implicated in human health risks. However, their neurotoxic mechanisms remain poorly understood. This study aims to investigate how MPCs contribute to neurodegenerative diseases, focusing on Alzheimer's (AD) and Parkinson's (PD) diseases as critical models. Using computational toxicology approaches, we screened 12 types of MPCs via SwissADME, identifying four representative MPCs with significant blood-brain barrier permeability and neurotoxic potential. Network toxicology (SwissTargetPrediction, ChEMBL) and protein interaction analysis (STRING, Cytoscape) revealed MPC-related AD/PD targets, including MAPK8 and SLC6A3, which were further validated through molecular docking (AutoDock). Key pathways-neuronal apoptosis and G protein-coupled receptor (GPCR) signaling-were disrupted by MPCs interactions, as evidenced by Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses. Notably, MPCs exhibited strong binding affinities to MAPK8 and SLC6A3, implicating these targets in neurodegeneration. Our findings establish a novel mechanistic link between environmental MPCs exposure and AD/PD pathogenesis, highlighting apoptosis dysregulation and GPCR signaling interference as central pathways. This work provides critical insights for policymakers and clinicians, underscoring the urgency of regulating MPCs to mitigate neurodegenerative risks and informing targeted therapeutic strategies.
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