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• W3119187345 abstract "Pathological changes involving TDP-43 protein (‘TDP-43 proteinopathy’) are typical for several neurodegenerative diseases, including frontotemporal lobar degeneration (FTLD). FTLD-TDP cases are characterized by increased binding of TDP-43 to an abundant lncRNA, NEAT1, in the cortex. However it is unclear whether enhanced TDP-43-NEAT1 interaction represents a protective mechanism. We show that accumulation of human TDP-43 leads to upregulation of the constitutive NEAT1 isoform, NEAT1_1, in cultured cells and in the brains of transgenic mice. Further, we demonstrate that overexpression of NEAT1_1 ameliorates TDP-43 toxicity in Drosophila and yeast models of TDP-43 proteinopathy. Thus, NEAT1_1 upregulation may be protective in TDP-43 proteinopathies affecting the brain. Approaches to boost NEAT1_1 expression in the CNS may prove useful in the treatment of these conditions." @default.
• W3119187345 created "2021-01-18" @default.
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• W3119187345 date "2021-01-11" @default.
• W3119187345 modified "2023-10-15" @default.
• W3119187345 title "Long non-coding RNA NEAT1_1 ameliorates TDP-43 toxicity in in vivo models of TDP-43 proteinopathy" @default.
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• W3119187345 doi "https://doi.org/10.1080/15476286.2020.1860580" @default.
• W3119187345 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8583295" @default.
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• W3119187345 hasPublicationYear "2021" @default.
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