ArticleNeurotoxicity research2025
Mechanistic Analysis of Decabromodiphenyl Ether-Induced Neurotoxicity in Humans Using Network Toxicology and Molecular Docking.
Article in Neurotoxicity research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Computational modeling for rational design of novel phenoxy tacrine derivatives targeting Alzheimer's disease.PloS one · 2026Article
- Evaluation of neurotoxicity of drugs from morphological and electrophysiological endpoints using human iPSC-derived neural cell models.Frontiers in cellular and infection microbiology · 2026Article
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
Commercial decabromodiphenyl ether (c-decaBDE) is a widely used additive flame retardant in textiles and plastics. This formulation predominantly consists of the congener BDE-209, with trace amounts of other brominated diphenyl ether congeners, such as nonabromodiphenyl ether and octabromodiphenyl ether. Recognized as a persistent organic pollutant due to its potential for long-range environmental transport, c-decaBDE poses significant environmental threats and serious human health risks, including endocrine, reproductive, developmental, and neurotoxic effects. The mechanisms underlying its neurotoxicity remain largely undefined. This study investigates the neurotoxic effects of BDE-209 in humans through network toxicology, multi-level bioinformatics approaches, and molecular docking analyses. Prediction results indicate that BDE-209 can cross the blood-brain barrier, entering the central nervous system and inducing neurotoxic effects. A comprehensive analysis has identified 294 potential targets linked to the neurotoxicity induced by BDE-209. Gene-gene interaction and pathway enrichment analyses revealed significant associations related to cellular responses to chemical stress and synaptic transmission. Further investigation of protein-protein interactions, combined with centrality analysis, identified 14 hub targets, including CaMK-II alpha, PSD-95, GluR-1, and GluN2B, as key proteins in this process. Molecular docking results indicate that BDE-209 exhibits a stronger binding affinity to GluN2B, a subunit of the N-methyl-D-aspartate (NMDA) receptors, compared to other key targets. These findings suggest that BDE-209 may disrupt the function of GluN2B-containing NMDA receptors, potentially leading to their inhibition. Such inhibition could result in reduced excitatory neurotransmission, impairing synaptic potentiation and plasticity, and ultimately contributing to neurotoxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.