I posted this on another thread, but I felt it needed a topic of its own. I was watching the video from 2017 on the found my fitness channel with the late Judith Campisi and I heard a couple of nuggets of infromation I thought I should check out and found the following results.
This to me raises major concerns about the reliabilty of the wormbots screening. Testing anything with potentially senolytic effects on the wormbot needs a response to this issue.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC693382/
Adult activity: C. elegans germline stem cells divide in the adult animal. No other cells divide in the adult.
and
The extent to which the primary causes of aging in C. elegans are the same or different to those in humans will only become clear once both are fully understood. However, it is already evident that C. elegans and mammals share some but not all senescent etiologies. For example, in mammals stem cell exhaustion (Shaw et al., 2010; Conboy and Rando, 2012) and accumulation of senescent cells (van Deursen, 2014) (sensu Hayflick; note that there are two distinct meanings of the word senescence ) contribute to senescence in the broad sense. By contrast, in adult C. elegans somatic cells are post-mitotic, and cellular senescence (sensu Hayflick) does not seem to occur. By contrast, interventions reducing insulin/IGF-1 or mTOR (mechanistic target of rapamycin) signaling or supporting protein folding homeostasis protect against aging in C. elegans and mammals (Zhang and Cuervo, 2008; Kenyon, 2010; Labbadia and Morimoto, 2014). Moreover, interventions causing loss of antioxidant defense or mitochondrial impairment which cause death in mammals can increase lifespan in C. elegans (Rea, 2005; Van Raamsdonk and Hekimi, 2009).
particularly:
By contrast, in adult C. elegans somatic cells are post-mitotic, and cellular senescence (sensu Hayflick) does not seem to occur.