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- W4300664751 abstract "Accumulating evidence has shown that Tau aggregates not only seed further tau aggregation within neurons but may also spread to neighboring cells and functionally connected brain regions. This process is referred to as “Tau propagation” and may explain the stereotypic progression of Tau pathology in the brains of Alzheimer’s disease (AD) patients. Tau filaments have distinct cellular and neuroanatomical distributions with morphological and biochemical differences, suggesting the ability to adopt disease-specific molecular conformations. These conformers may give rise to different neuropathological phenotypes, reminiscent of prion strains (strain hypothesis). Autophagy is one of the surveillance systems that contribute to protein homeostasis (proteostasis) through their degradation in lysosomes. The loss of proteostasis occurs with age and in neurodegenerative diseases, such as AD. Defective autophagy has been proposed to contribute to the accumulation of protein aggregates in the elderly brain and as well as the brains of patients with neurodegenerative conditions. In this chapter, we discuss the different Tau propagation mechanisms that may be involved in the cell-to-cell transmission of AD and related tauopathies. The mechanisms by which deficits in autophagic degradative pathways may contribute to the abnormal accumulation of tau in AD are also considered. Furthermore, the issue of pharmacological agents targeting specific tau species to promote the autophagic clearance of Tau from cells will be addressed. We propose our hypothesis that strain-specific autophagic degradation may contribute to the pathogenesis of tauopathies." @default.
- W4300664751 created "2022-10-04" @default.
- W4300664751 creator A5043338037 @default.
- W4300664751 creator A5078924905 @default.
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- W4300664751 date "2022-01-01" @default.
- W4300664751 modified "2023-09-24" @default.
- W4300664751 title "Tau propagation and autophagy" @default.
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- W4300664751 doi "https://doi.org/10.1016/b978-0-323-89906-2.00014-9" @default.
- W4300664751 hasPublicationYear "2022" @default.
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