Two human metabolites rescue a C. elegans model of Alzheimer’s disease via a cytosolic unfolded protein response

Joshi et al. identify two human metabolites, carnosine and kynurenic acid, that rescue a C. elegans model of Alzheimer’s disease by inhibiting the aggregation of the amyloid beta peptide in vivo. They find that these metabolites trigger a cytosolic unfolded protein response through the transcription...

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Autores principales: Priyanka Joshi, Michele Perni, Ryan Limbocker, Benedetta Mannini, Sam Casford, Sean Chia, Johnny Habchi, Johnathan Labbadia, Christopher M. Dobson, Michele Vendruscolo
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/b28a52b5717142fcbc1079229aedf157
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Sumario:Joshi et al. identify two human metabolites, carnosine and kynurenic acid, that rescue a C. elegans model of Alzheimer’s disease by inhibiting the aggregation of the amyloid beta peptide in vivo. They find that these metabolites trigger a cytosolic unfolded protein response through the transcription factor HSF-1 and molecular chaperones DNJ-12 and DNJ-19, thus providing mechanistic links between metabolite homeostasis and protein homeostasis to further insights into interventions against neurodegenerative diseases.