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- W4225097384 abstract "Recent evidence links dysfunctional lipid metabolism to the pathogenesis of Parkinson's disease, but the mechanisms are not resolved. Here, we created a new Drosophila knock-in model of DNAJC6/Auxilin and find that the pathogenic mutation causes synaptic dysfunction, neurological defects and neurodegeneration, as well as specific lipid metabolism alterations. In these mutants membrane lipids containing long-chain polyunsaturated fatty acids, including phosphatidylinositol lipid species that are key for synaptic vesicle recycling and organelle function are reduced. Overexpression of another protein mutated in Parkinson's disease, Synaptojanin-1, known to bind and synthesize specific phosphoinositides, strongly rescues the DNAJC6/Auxilin neuronal defects and neurodegeneration. Our work reveals a functional relation between two proteins mutated in Parkinson's disease and implicates deregulated phosphoinositide metabolism in the maintenance of neuronal integrity and neuronal survival in Parkinsonism." @default.
- W4225097384 created "2022-04-30" @default.
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- W4225097384 date "2022-04-28" @default.
- W4225097384 modified "2023-10-12" @default.
- W4225097384 title "Parkinson mutations in DNAJC6 cause lipid defects and neurodegeneration that are rescued by Synj1" @default.
- W4225097384 doi "https://doi.org/10.1101/2022.04.27.489745" @default.
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