Maybe, maybe not. More research is needed.

Through metabolic screening, we identified uridine as a potential regulator to rejuvenate aged HSPCs.

Here we examined whether IL-11, a pro-inflammatory cytokine of the IL-6 family, has a negative effect on age-associated disease and lifespan.

Researchers publishing in Aging have found a molecule linking exercise to the inhibition of cellular senescence, one of the hallmarks of aging.

The researchers investigated whether NAD precusors, including nicotinamide and NR, along with the well-known compound rapamycin could rescue mitophagy, and they found positive results for all of these compounds.

TAC promoted tissue rejuvenation, including new neuron formation, and alleviated multiple aging hallmarks in aged mice, revealing the regenerative potential of adult tissues through physiological TERT activation.

The authors elaborate on the potential mechanisms underlying the connection between oral microbial dysbiosis and cognitive function impairment.

16α-hydroxyestriol was the star of this study, producing a 15% increase in median lifespan in male mice. However, it lowered median lifespan in females by 7%. While many drugs affect lifespan sex-specifically, opposing effects are rare; in fact, this is the first case in ITP’s history. Interestingly, we have another example from the same study: canagliflozin, when started at 16 months of age, led to a 14% increase in median lifespan in males and a 6% decline in females. In a previous ITP study, when started at 6 months, canagliflozin increased male lifespan without affecting female lifespan. All other tested drugs did not have a statistically significant effect on lifespan in either sex.