Aging as an event of proteostasis collapse

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Taylor, Rebecca C. and Dillin, Andrew (2011) Aging as an event of proteostasis collapse. Cold Spring Harbor Perspectives in Biology, 3 (5). pp. 1-17. ISSN 1943-0264

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Abstract

Aging cells accumulate damaged and misfolded proteins through a functional decline in their protein homeostasis (proteostasis) machinery, leading to reduced cellular viability and the development of protein misfolding diseases such as Alzheimer's and Huntington's. Metabolic signaling pathways that regulate the aging process, mediated by insulin/IGF-1 signaling, dietary restriction, and reduced mitochondrial function, can modulate the proteostasis machinery in manyways to maintain a youthful proteome for longer and prevent the onset of age-associated diseases. These mechanisms therefore represent potential therapeutic targets in the prevention and treatment of such pathologies.

Item Type:	Article
Uncontrolled Keywords:	biochemistry, genetics and molecular biology(all) ,/dk/atira/pure/subjectarea/asjc/1300
Related URLs:	http://www.scopus.com/inward/record.url?...
Depositing User:	LivePure Connector
Date Deposited:	13 Feb 2025 17:30
Last Modified:	16 Feb 2025 07:30
URI:	https://ueaeprints.uea.ac.uk/id/eprint/98489
DOI:	10.1101/cshperspect.a004440

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