Aging Phenotype Assessment
Objective: Comprehensive evaluation of structural and functional aging phenotypes across multiple physiological systems to determine whether rapamycin slows the rate of aging in mice
Protocol Steps
Study Design Setup
Comprehensive, large-scale assessment of a wide range of structural and functional aging phenotypes was performed on male C57BL/6J mice
Note: Study included both young and aged animals to determine if rapamycin effects were aging-dependent or aging-independent
View evidence from paper
“comprehensive, large-scale assessment of a wide range of structural and functional aging phenotypes, which we performed to determine whether rapamycin slows the rate of aging in male C57BL/6J mice”
Treatment Administration
Rapamycin (FDA-approved mTOR inhibitor) was administered to mice as part of the intervention
Note: Rapamycin is an mTOR inhibitor that was previously reported to extend lifespan in mammals
View evidence from paper
“The recent report of lifespan extension in mice treated with the FDA-approved mTOR inhibitor rapamycin represented the first demonstration of pharmacological extension of maximal lifespan in mammals”
Phenotype Assessment
Multiple aging phenotypes were evaluated across structural and functional domains
Note: Assessment included evaluation of aging traits to determine if rapamycin ameliorated aging phenotypes
View evidence from paper
“While rapamycin did extend lifespan, it ameliorated few studied aging phenotypes. A subset of aging traits appeared to be rescued by rapamycin”
Age-Dependent Effect Analysis
Comparison of rapamycin effects in young versus aged animals to distinguish aging-dependent from aging-independent drug effects
Note: Rapamycin had similar effects on many traits in young animals, indicating effects were not due to modulation of aging but rather aging-independent drug effects
View evidence from paper
“Rapamycin, however, had similar effects on many of these traits in young animals, indicating that these effects were not due to a modulation of aging, but rather related to aging-independent drug effects”