‘It raises the tantalising possibility that the drugs could have a similar effect in elderly humans,’ study author professor Stuart Cook said.
Scientists have extended the lifespans of mice by about 25 percent by blocking a protein called interleukin-11 (IL-11), showing promise for slowing down human aging, according to a study published in Nature on July 17.
Professor Stuart Cook, a co-corresponding author in the study, said in a statement that previously proposed life-extending drugs and treatments have either had poor side effects, failed to work in both sexes, or “could extend life, but not healthy life.”
“This does not appear to be the case for IL-11,” Mr. Cook said. “While these findings are only in mice, it raises the tantalising possibility that the drugs could have a similar effect in elderly humans.”
While IL-11 is important in some animal species such as fish and tadpoles for regenerating limbs and lost organs, it is believed to be largely redundant in humans.
Researchers wanted to see if blocking the protein could not only increase the lifespan of mice but also affect their health and susceptibility to certain illnesses.
“Ageing studies to date have focused largely on lifespan extension, particularly in yeast, worms and fruit flies, but lifespan extension does not necessarily reflect longer healthspan,” the researchers wrote. “There is a need for integrated studies to determine the effects of interventions on both healthspan and lifespan.”
Researchers noted that laboratory mice are particularly suited for lifespan extension experiments because aging pathologies that are “important for human wellbeing and function” are also apparent in mice and lifespan studies in the animals are well established.
Mice Lived Longer, Were Healthier
In the study, researchers found that administering anti-IL-11—a manufactured antibody that neutralizes the protein—to 75-week-old mice (the human equivalent of approximately 55 years of age) for 25 weeks improved metabolism and muscle function and reduced aging biomarkers and frailty in both male and female mice.
Meanwhile, in lifespan studies, genetically deleting the IL-11-producing gene in mice extended the lives of both males and females by 24.9 percent on average, the researchers found.
Male mice treated with anti-IL-11 from 75 weeks of age until death saw their median lifespan extended by 22.5 percent, while female mice treated with anti-IL-11 from the same age until death had their median lifespan extended by 25 percent.
The mice lived for an average of 155 weeks, compared with 120 weeks in untreated mice, researchers found.
Additionally, researchers found that inhibition of IL-11 in mice “significantly reduces” deaths from age-related cancers, multiple diseases caused by fibrosis, and chronic inflammation.
There were also few side effects observed, researchers said.
Human Trials
“Together, these results demonstrate a role for the pro-inflammatory factor IL-11 in mammalian healthspan and lifespan,” researchers wrote.
It is not yet clear if the same results could be seen in humans, although an anti-IL-11 antibody drug is currently being trialed in patients with lung fibrosis, according to researchers.
Clinical trials of the anti-IL-11 drug in combination with immunotherapy to treat cancer are also planned, they said.
“We suggest that anti-IL-11 therapy, which is currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people,” the researchers said.