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Inhibiting inflammatory protein extends lifespan

Wishing for a happy, healthy and extended lifespan could soon become more than just wishful thinking, if the latest findings from a new research on mice models are successfully translated in people.

Scientists at the Medical Research Council (MRC) Laboratory of Medical Science, and Imperial College London have discovered that ‘switching off’ a protein called interleukin 11 (IL-11) significantly increased the healthy lifespan of mice by almost 25 percent. The scientists, working with colleagues at Duke-NUS Medical School in Singapore, tested the effects of IL-11 by creating mice that had the gene producing IL-11 deleted. This extended the lives of the mice by over 20 percent on average.

They also treated 75-week-old mice — equivalent in human terms to the age of about 55 years — with an injection of an anti-IL-11 antibody, a drug which stops the effects of the IL-11 in the body. The outcome of the tests was nothing short of phenomenal, with mice given the anti-IL-11 drug from 75 weeks of age until death having their median lifespan extended by 22.4 percent in males and 25 percent in females. The treated mice lived for an average of 155 weeks, compared with 120 weeks in untreated mice.

The administration of anti-IL-11 in the rats also significantly reduced deaths from cancer and many diseases caused by poor metabolism, fibrosis, and chronic inflammation, all of which are hallmarks of aging. In other words, the old mice receiving anti-IL-11 were not only living longer they were also enjoying a healthier old age with reduced muscle wasting and improvement in muscle strength. The scientists also observed very few side effects among the treated mice.

Life-extending drugs and treatments that were proposed earlier, were found to have several shortcomings, including serious side-effects, not being effective on both genders, or extending life but not a healthy life. The treatment with IL-11 did not have any of these limitations. The researchers noted that while their findings were currently limited to mice, the study raised the tantalizing possibility that the anti-IL-11 drug could have a similar effect in elderly humans.

Previous research has shown that in humans, after about the age of 55, more IL-11 is produced in the body and that this increase was linked to chronic inflammation, fibrosis in organs, disorders of metabolism, muscle wasting (sarcopenia), frailty, and cardiac fibrosis. These conditions are many of the signs associated with aging.
Anti-IL-11 treatments are currently in human clinical trials for other conditions, potentially providing opportunities to study its effects in aged people in the future.

When two or more age-related health conditions occur in an individual, it is known as multimorbidity, which encompasses a range of conditions including lung disease, cardiovascular disease, diabetes, vision and hearing decline and a host of other conditions. Currently, no treatment for multimorbidity is available, other than to try to treat the separate multiple underlying causes individually.








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