Mannick has studied the effects of rapamycin-like drugs in Covid-19. Her trial took place in nursing homes where the disease broke out. For four weeks, half of the participants received the drug, while the other half received a placebo. Of those given a placebo, “25 percent of them developed severe covid and half died,” said Mannick, who has yet to publish the work. None of those taking the drug developed symptoms of Covid-19.
“There are multiple strategies to help the aging immune system better fight Covid,” she says. “Aging is the biggest risk factor for severe covid, and it’s a modifiable risk factor.”
She hopes to extend the use of her drug beyond Covid-19; a rejuvenated immune system could theoretically ward off many other viral and bacterial infections. Her colleague Stanley Perlman, a coronavirus virologist at the University of Iowa who co-authored BioAge’s covid drug study in mice, has future pandemics in mind. “The next time there is another coronavirus in 2030, all this information might be very helpful,” he says.
Get rid of the old
The immune system is not the only target of anti-aging drugs. Others focus on clearing out senescent cells. Most cells in our body divide to some degree. Once they reach this limit, they must die and be cleared out by the immune system. But that’s not always the case – some cells stick around. These cells no longer divide, and some instead produce a toxic concoction of chemicals that cause harmful inflammation in the environment and beyond.
Cells that do this are called “aged” and they build up in our organs as we age. They have been linked to an ever-growing number of age-related diseases, including diabetes, heart disease, osteoporosis, cataracts, Alzheimer’s – the list goes on. They also appear to play an important role in infections with the corona virus.
In research yet to be published, James Kirkland, who studies aging and cell aging at the Mayo Clinic in Rochester, Minnesota, says he has evidence that coronavirus infects aging cells faster than non-aging cells. His research also suggests that senescent cells release chemicals that cause neighboring non-senescent cells to also take up the virus, he says.
These cells not only absorb more coronavirus, but they also turn out to be a breeding ground for new virus variants† “There is mounting evidence that senescent cells infected with coronavirus can mutate that virus,” Kirkland says. “So they may even be a cause of viral mutations.”
As an extra concern, the coronavirus can age healthy cells. Given all of this, senescence has become a clear target of both anti-aging and covid-19 therapies. Studies in mice and hamsters suggest that: compounds that kill senescent cells may improve symptoms of covid-19 and increase the chances of survival.