Mannick has investigated the effects of rapamycin-like drugs in covid-19. Her trial has taken place in nursing homes that have experienced outbreaks of the disease. For four weeks, half of the participants received the medication, while the other half received placebo. Among those who received placebo, “25% of them developed severe covid, and half of them died,” says Mannick, who has not yet published the work. None of those taking the drug developed any covid-19 symptoms.
“There are several strategies to help the aging immune system fight covid better,” she says. “Aging is the major risk factor for severe covid, and it is a modifiable risk factor.”
She hopes to expand 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 coronavirologist at the University of Iowa who co-authored the research on BioAge’s covid drug in mice, has future pandemics in mind. “Next time there is another coronavirus in 2030, all this information might be very useful,” he says.
Out with the old
The immune system is not the only target for anti-aging drugs. Others aim at clear out old cells. Most of the cells in our body divide up to a certain point. When they reach this limit, they should die and be cleared away by the immune system. But this is not always the case – some cells get stuck. These cells no longer divide, and some instead secrete a toxic brew of chemicals that trigger harmful inflammation in the surrounding area and beyond.
Cells that do this are called “aging” and they accumulate across our organs as we age. They have been linked to an ever-increasing number of age-related diseases, including diabetes, heart disease, osteoporosis, cataracts, the Alzheimer’s list continues. They also appear to play an important role in coronavirus infections.
In as yet unpublished research, James Kirkland, who studies aging and cell aging at the Mayo Clinic in Rochester, Minnesota, says he has evidence that coronavirus infects senescence cells faster than non-aging cells. His research also suggests that aging cells release chemicals that cause neighboring cells to take up the virus, he says.
Not only do these cells take on more coronavirus, but they also appear to provide fertile ground for new virus variants. “There is new evidence that coronavirus-infected tendon cells can mutate that virus,” Kirkland said. “So they may even be a cause of viral mutations.”
As an added concern, coronavirus can cause healthy cells to age. In view of all this, old age has become an obvious target for both anti-aging and covid-19 therapies. Studies on mice and hamsters suggest this compounds that kill senescent cells may improve the symptoms of covid-19 and increase the chances of survival.