Gene B. Hubbard

TL;DR: It is demonstrated that transplanting relatively small numbers of senescent cells into young mice is sufficient to cause persistent physical dysfunction, as well as to spread cellular senescence to host tissues, and a senolytic can reverse this dysfunction and potently increase lifespan in aged mice.

TL;DR: It is shown that rapamycin selectively blunts the pro-inflammatory phenotype of senescent cells, which might ameliorate age-related pathologies, including late-life cancer, by suppressing senescence-associated inflammation.

TL;DR: The authors' data illustrate the complexity of CR in the context of aging, with a clear separation of outcomes related to health and survival, highlighting complexities of translation of CR into human interventions.

TL;DR: It is found that the incidence of presumably fatal adenocarcinoma in lung was significantly lower in Ames dwarf mice than for their normal siblings and possibly could be attributed to the retardation of tumor development by changes in the levels of growth hormone and insulin-like growth factor-1, and thereby be a major contributing factor to the extended life span observed in these mice.

TL;DR: It is found that Myc haploinsufficient (Myc(+/-) mice exhibit increased lifespan and appear to be more active, with a higher metabolic rate and healthier lipid metabolism, and a gene expression signature enriched for metabolic and immune processes.