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- W2022792702 abstract "Abstract Neuroinflammation is a striking hallmark of amyotrophic lateral sclerosis (ALS) and other neurodegenerative disorders. Previous studies have shown the contribution of glial cells such as astrocytes in TDP-43-linked ALS. However, the role of microglia in TDP-43-mediated motor neuron degeneration remains poorly understood. In this study, we show that depletion of TDP-43 in microglia, but not in astrocytes, strikingly upregulates cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) production through the activation of MAPK/ERK signaling and initiates neurotoxicity. Moreover, we find that administration of celecoxib, a specific COX-2 inhibitor, greatly diminishes the neurotoxicity triggered by TDP-43-depleted microglia. Taken together, our results reveal a previously unrecognized non-cell-autonomous mechanism in TDP-43-mediated neurodegeneration, identifying COX-2-PGE2 as the molecular events of microglia- but not astrocyte-initiated neurotoxicity and identifying celecoxib as a novel potential therapy for TDP-43-linked ALS and possibly other types of ALS." @default.
- W2022792702 created "2016-06-24" @default.
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- W2022792702 date "2015-03-26" @default.
- W2022792702 modified "2023-10-14" @default.
- W2022792702 title "Induction of COX-2-PGE2 synthesis by activation of the MAPK/ERK pathway contributes to neuronal death triggered by TDP-43-depleted microglia" @default.
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- W2022792702 doi "https://doi.org/10.1038/cddis.2015.69" @default.
- W2022792702 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4385945" @default.
- W2022792702 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25811799" @default.
- W2022792702 hasPublicationYear "2015" @default.
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