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- W1567497774 abstract "Tauopathies, such as Alzheimer's disease (AD) and Frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), are characterized by tau accumulation. This accumulation could result from alterations in tau degradation by either the ubiquitin-proteasome system or the autophagy-lysosomal pathway. To analyze a possible alteration of the autophagy-lysosomal pathway in transgenic mice expressing human tau with three FTDP-17 missense mutations (TauVLW mice), we studied the lysosomal enzyme Cathepsin D. The hippocampi of TauVLW mice, where the human mutant tau accumulates, showed both increased Cathepsin D and partial colocalization of Cathepsin D with human mutant tau. At the ultrastructural level, some multivesicular bodies showed human mutant tau-immunopositive vesicles. This finding could provide insights into the molecular mechanisms of tau degradation in human tauopathies." @default.
- W1567497774 created "2016-06-24" @default.
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- W1567497774 date "2015-03-03" @default.
- W1567497774 modified "2023-09-23" @default.
- W1567497774 title "Cathepsin D in a Murine Model of Frontotemporal Dementia with Parkinsonism-Linked to Chromosome 17" @default.
- W1567497774 doi "https://doi.org/10.3233/jad-140456" @default.
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