Glucose delays age‐dependent proteotoxicity

Aging Cell

Arnaud Tauffenberger¹  Alexandra Vaccaro¹  Anais Aulas¹  Christine Vande Velde¹ 

[1] CRCHUM

关键词: aging;    Caenorhabditis elegans;    metabolism;    neurodegeneration;    protein folding;    proteotoxicity;   

DOI  :  10.1111/j.1474-9726.2012.00855.x

来源: Wiley

【 摘 要 】

Summary

Nutrient availability influences an organism’s life history with profound effects on metabolism and lifespan. The association between a healthy lifespan and metabolism is incompletely understood, but a central factor is glucose metabolism. Although glucose is an important cellular energy source, glucose restriction is associated with extended lifespan in simple animals and a reduced incidence of age-dependent pathologies in humans. We report here that glucose enrichment delays mutant polyglutamine, TDP-43, FUS, and amyloid-β toxicity in Caenorhabditis elegans models of neurodegeneration by reducing protein misfolding. Dysregulated metabolism is common to neurodegeneration and we show that glucose enrichment is broadly protective against proteotoxicity.

【 授权许可】

Unknown   
© 2012 The Authors. Aging Cell © 2012 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland