Eva Gómez‐Orte

This study shows that loss of mitochondrial glutathione reductase and thioredoxin reductase in C. elegans causes growth, fertility, and muscle defects, activates a constitutive UPRmt, and alters mitochondrial morphology.

The paper shows that inactivating the NMD pathway suppresses the embryonic lethality of gsr-1 mutants in C. elegans by enabling the transsulfuration pathway to compensate for the loss of glutathione reductase function.

The paper characterizes molecular markers during in vitro adult neurogenesis in Alzheimer's disease by analyzing gene expression changes in neural progenitor cells exposed to Aβ1-42.