Glucose delays age-dependent proteotoxicity.
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.
CRCHUM, Université de Montréal, Montréal, Québec, Canada.
Arnaud
A
Tauffenberger
Alexandra
A
Vaccaro
Anais
A
Aulas
Christine
C
Vande Velde
J Alex
JA
Parker
D000367:Age Factors; D000818:Animals; D017173:Caenorhabditis elegans / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism*; D031204:Caloric Restriction; D004195:Disease Models, Animal; D005947:Glucose / Q000008:administration & dosage* / Q000378:metabolism; D008136:Longevity; D019636:Neurodegenerative Diseases / Q000139:chemically induced / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D017510:Protein Folding; D059748:Proteolysis; D057165:Proteostasis Deficiencies / Q000139:chemically induced / Q000378:metabolism*
D029742:Caenorhabditis elegans Proteins; D005947:Glucose