Peter de Keizer, a molecular geneticist at Erasmus University, reports in the journal Cell that he and his colleagues have developed a technique that kills off senescent cells. Our bodies have two ways of preventing damaged cells from becoming cancerous: kill them off, or cause them to cease replication and thus become senescent. Senescent cells accumulate as we grow older, secreting inflammatory substances that harm neighboring cells and contribute to many age-related diseases, including atherosclerorsis and diabetes.
De Keizer and his colleagues have developed a treatment in mice that selectively kills senescent cells while leaving healthy normal cells alone. They discovered that old or damaged cells become senescent rather than die when the FOXO4 protein binds to the tumor suppressor gene p53. They have designed another protein that interferes with the ability of FOXO4 to halt p53 from causing cells to die.
De Keizer’s team administered the new protein to both fast-aging and normally aged mice. The treatment worked as they had hoped, jumpstarting the ability of p53 to make senescent cells commit suicide. Eliminating senescent cells restored stamina, fur density, and kidney function in both strains of mice. The researchers report that they are continuing to study the rodents to see if the treatment extends their lifespans. They plan to try the treatment to stop brain cancer in human beings, but the ultimate goal is to treat aging as a disease. “Maybe when you get to 65 you’ll go every five years for your anti-senescence shot in the clinic. You’ll go for your rejuvenation shot,” de Keizer told the Tech Times.
In the same week, another group of Harvard researchers led by molecular biologist David Sinclair reported in Science about experiments in mice that thwart DNA damage associated with aging and exposure to radiation. As we age, our cells lose their ability to repair the damage to the DNA that makes up our genes. The repair process is orchestrated by the SIRT1 and PARP1 proteins. Both proteins consume the ubiquitous coenzyme nicotinamide adenine dinucleotide (NAD) to operate. As we grow older, the amount of NAD in our cells declines, thus allowing another protein, DBC1, to inhibit the DNA repair activity of both SIRT1 and PARP1.
I’m taking Niagen, which contains the NAD precursor nicotinamide riboside. How well does it work? I have no side effects that I can identify, and my workouts seem to have been more productive since I started taking it, but really there’s no way to tell if it’s slowing aging or not.