Protein homeostasis and aging in neurodegeneration

Peter M. Douglas, Andrew Dillin

Research output: Contribution to journalReview article

202 Scopus citations

Abstract

Genetic and environmental factors responsible for numerous neurodegenerative diseases vary between disorders, yet age remains a universal risk factor. Age-associated decline in protein homeostasis, or proteostasis, enables disease-linked proteins to adopt aberrant tertiary structures, accumulate as higher-ordered aggregates, and cause a myriad of cellular dysfunctions and neuronal death. However, recent findings suggest that the assembly of disease proteins into tightly ordered aggregates can significantly delay proteotoxic onset. Furthermore, manipulation of metabolic pathways through key signaling components extends lifespan, bolsters proteostasis networks, and delays the onset of proteotoxicity. Thus, understanding the relationship between proteostasis and aging has provided important insights into neurodegeneration.

Original languageEnglish (US)
Pages (from-to)719-729
Number of pages11
JournalJournal of Cell Biology
Volume190
Issue number5
DOIs
StatePublished - Sep 6 2010

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ASJC Scopus subject areas

  • Cell Biology

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