Our findings demonstrate lifespan-extending diets repress miRNA-chromatin remodeler interactions and safeguard against deregulated transcription induced by aging and lifespan shortening diets, events linked by microRNA, chromatin, and ncRNA crosstalk.
In addition, an augmented and completed study demonstrates lifespan extension in male Irs1 null mice.
Confirming earlier studies by the Helfand lab, which demonstrated lifespan extension when dominant-negative p53 is expressed in neurons [ 16- 18], Waskar and colleagues find that ubiquitous expression of a dominant negative form of p53 extends lifespan moderately in females [ 12].
Recent advances demonstrate that lifespan can be increased, and health improved by treating model organisms with drugs that target intracellular signalling pathways (Kennedy and Pennypacker 2013).
Our study demonstrated its lifespan prolonging, anti-stress and anti-proteotoxicity effects in an organism.
The SAMP8 mouse demonstrates reduced lifespan compared to control normal-aging SAMR1 mice [76] as well as age-related cognitive decline in a manner reminiscent of Alzheimer's disease [77], [78].
This demonstrates that lifespan extending treatments are not purely rescuing weak backgrounds.
Survival curves for the remaining Canton-S adults demonstrated that lifespan decreased as radiation dose increased (Fig. 2).
A separate study demonstrated that lifespan can be extended in C. elegans by pharmacologically altering adrenoceptor, histamine, serotonin, dopamine, or octopamine signaling.
We previously demonstrated significant lifespan extension in neoplasia‐prone Rb+/− and Apc Min/+ mice (Livi et al., 2013; Hasty et al., 2014).
As rdgA (Drosophila DGK) mutants demonstrated increased lifespan and lowered p-S6K levels (Fig. S3A,B, Supporting information), we examined whether C. elegans dgk-5 mutants also present the similar phenotypes.
