ArticleEnvironment & health (Washington, D.C.)2026
Imbalance of the Arachidonic Acid Metabolism in Neuroinflammation and Cognition Caused by Manganese Exposure: Downregulation of 15d-PGJ2 Levels and Validation of MMP9 as a Target.
Article in Environment & health (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Downregulation of the L-PGDS/15d-PGJ2 Pathway Is Associated with Manganese-Induced Neuroinflammation and Cognitive Impairment Involving C/EBPβ and MMP9.Antioxidants (Basel, Switzerland) · 2026Article
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11 authors.
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Abstract
Exposure to manganese (Mn) is known to induce cognitive dysfunction, but the underlying processes involving neuroinflammation and arachidonic acid (AA) metabolism remain incompletely understood. This study integrates human epidemiological data with experimental models to elucidate these pathways and identify potential therapeutic targets. First, in a cross-sectional study of Mn-exposed workers, we observed elevated serum levels of pro-inflammatory cytokines and dysregulated expression of mRNAs related to AA metabolism, both of which were identified as important mediators between Mn exposure and cognitive impairment. In mouse models, multilevel analyses combining behavioral assays, striatal transcriptomics, and oxidized lipid metabolomics demonstrated that Mn exposure triggers microglial activation, disrupts AA metabolic pathways, and drives neuroinflammation, culminating in cognitive impairment. A central finding was the downregulation of 15-deoxy-Δ
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