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- W1424503539 endingPage "411" @default.
- W1424503539 startingPage "391" @default.
- W1424503539 abstract "Despite the differences, Alzheimer's disease (AD)—a chronic neurodegenerative disease of late age—and Niemann–Pick type C disease (NPC)—an inherited storage disorder of early childhood—share pathological features including neurodegeneration, neurofibrillary abnormalities, and P-amyloid accumulation. In both the disorders, the endocytic pathway function is prominently impaired. Moreover, disease onset is promoted by inheritance of the ɛ4 isoform of apolipoprotein-E, a major carrier protein for cholesterol, suggesting that cholesterol mishandling plays a role in AD as well as NPC. This chapter reviews the cell biology underlying the defects in these disorders with special emphasis on dysfunction of the endocytic pathway and lysosomal system. The chapter addresses how faulty lipid trafficking and alterations of the Rab proteins associated with early- and late-stage endocytic compartments—that is, Rabs 4, 7, and 9—may disrupt vesicular transport leading to altered sorting, accumulation of endosomal cargos, and impaired net movement of late endosomal compartments. The redistribution of lysosomal proteases among different types of endocytic organelles and its relevance to the altered metabolism of amyloid-β precursor protein and amyloid-β formation are also considered in the chapter." @default.
- W1424503539 created "2016-06-24" @default.
- W1424503539 creator A5022090615 @default.
- W1424503539 creator A5079303254 @default.
- W1424503539 date "2007-01-01" @default.
- W1424503539 modified "2023-09-26" @default.
- W1424503539 title "Neuronal Protein Trafficking in Alzheimer's Disease and Niemann-Pick Type C Disease" @default.
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