David Gems

This study shows that the longevity of C. elegans Eat mutants is mostly due to reduced bacterial infection rather than dietary restriction.

This study investigates how survival curve shapes change with aging in C. elegans and finds that rectangularization and triangularization reflect different patterns of healthspan and morbidity expansion.

This study shows that reducing insulin/IGF-1 signaling in early adulthood extends healthspan and lifespan, but in later life, it accelerates aging and reduces lifespan.

The paper shows that in C. elegans, lifespan is limited by competing senescent pathologies, and removing one can unmask another, indicating lifespan extension may not reflect reduced aging rate.

This study shows that autophagy gene knockdown in C. elegans affects lifespan in a highly condition-dependent manner, with variable outcomes based on genetic background, temperature, and experimental conditions.

This study challenges the assumption that reduced Gompertz parameter {beta} indicates decelerated aging by showing it results from expanded decrepitude in long-lived C. elegans.

The paper uses machine learning to predict lifespan and causes of death in aging C. elegans by analyzing senescent pathology and genetic factors.

The paper shows that C. elegans hermaphrodites undergo reproductive death after reproduction, which is suppressed by germline removal and linked to lifespan extension.

This study shows that C. elegans mothers transfer yolk to offspring via lactation, a process promoted by insulin/IGF-1 signalling, leading to reproductive death.

The paper introduces a label-free automated method to score nematode survival in high-throughput assays and finds an autophagy-dependent increase in acute stress resistance in early adulthood.

The paper investigates uterine tumors in C. elegans as a senescent pathology caused by quasi-programs, showing similarities to teratomas and senescence.

This study identifies autophagy-mediated gut-to-yolk biomass conversion as a cause of visceral pathologies and polymorbidity in aging C. elegans, and shows that inhibiting this process extends lifespan.