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- W2049557390 endingPage "2391" @default.
- W2049557390 startingPage "2376" @default.
- W2049557390 abstract "In order to successfully respond to stress all cells rely on the ability of the proteasomal and lysosomal proteolytic pathways to continually maintain protein turnover. Increasing evidence suggests that as part of normal aging there are age-related impairments in protein turnover by the proteasomal proteolytic pathway, and perturbations of the lysosomal proteolytic pathway. Furthermore, with numerous studies suggest an elevated level of a specialized form of lysosomal proteolysis (autophagy or macroautophagy) occurs during the aging of multiple cell types. Age-related alterations in proteolysis are believed to contribute to a wide variety of neuropathological manifestations including elevations in protein oxidation, protein aggregation, and cytotoxicity. Within the brain altered protein turnover is believed to contribute to elevations in multiple forms of protein aggregation ranging from tangle and Lewy body formation, to lipofuscin-ceroid accumulation. In this review we discuss and summarize evidence for proteolytic alterations occurring in the aging brain, the contribution of oxidative stress to disruption of protein turnover during normal aging, the evidence for cross-talk between the proteasome and lysosomal proteolytic pathways in the brain, and explore the contribution of altered proteolysis as a mediator of oxidative stress, neuropathology, and neurotoxicity in the aging brain." @default.
- W2049557390 created "2016-06-24" @default.
- W2049557390 creator A5011049890 @default.
- W2049557390 creator A5013418213 @default.
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- W2049557390 creator A5071329167 @default.
- W2049557390 creator A5072118430 @default.
- W2049557390 creator A5077965769 @default.
- W2049557390 date "2004-12-01" @default.
- W2049557390 modified "2023-10-14" @default.
- W2049557390 title "Autophagy, proteasomes, lipofuscin, and oxidative stress in the aging brain" @default.
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