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• W4320487079 startingPage "102249" @default.
• W4320487079 abstract "A-synuclein (α-syn) is a protein associated with the pathogenesis of Parkinson's disease (PD), a neurodegenerative disease with no effective treatment. Therefore, there has been a strong drive to clarify the pathology of PD associated with α-syn. Several mechanisms have been proposed to unravel the pathological cascade of this disease, and most of them share a particular similarity: cell-to-cell communication through exosomes (EXO). Here, we show that tumor necrosis factor receptor superfamily member 10B (TNFRSF10B) promotes the secretion of α-syn-containing EXO by microglia, resulting in motor dysfunction in PD. Upregulation of TNFRSF10B predicted severer condition in PD patients. In response to α-syn preformed fibrils (PFF), the expression of TNFRSF10B was increased in microglia. PFF-treated microglia exhibited a pro-inflammatory phenotype and caused neuronal damage by secreting α-syn-containing EXO. TNFRSF10B downregulation in microglia inhibited the secretion of α-syn-containing EXO and the release of pro-inflammatory factors, and ameliorated neuronal injury. PFF induced motor dysfunction in mice, which was ameliorated by inhibiting TNFRSF10B to suppress microglia-mediated α-syn communication or by directly depleting microglia. Taken together, these results indicate that TNFRSF10B promotes neuronal injury and motor dysfunction by delivery of α-syn-containing EXO and highlight the TNFRSF10B knockdown as a potential therapeutic target in PD." @default.
• W4320487079 created "2023-02-14" @default.
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• W4320487079 date "2023-04-01" @default.
• W4320487079 modified "2023-09-23" @default.
• W4320487079 title "TNFRSF10B is involved in motor dysfunction in Parkinson's disease by regulating exosomal α-synuclein secretion from microglia" @default.
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• W4320487079 doi "https://doi.org/10.1016/j.jchemneu.2023.102249" @default.
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• W4320487079 hasPublicationYear "2023" @default.
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