Image: a singularly terrifying poster image for The Curious Case of Benjamin Button
The eternal life of the future won’t have much to do with computers or “downloadable consciousness.” That’s just a clever set of exaggerations and distortions designed to sell books, and Google. The reality of artificial life extension will come from biotechnology, specifically stem cells, the cells in the body that haven’t yet become specialized and, thus, can become any number of different things with different physiological functions, like fighting disease—or aging. A study out today in an early edition of the journal Science essentially breaks this future wide open, describing a protein molecule that reverses aging effects at the genetic level in the hearts, brains, and skeletal muscles of mice. The effect is dramatic and, in a way, rather simple.
First, we need to step back one year to the release of a paper from a portion of same research team, based at Harvard University. That paper described experiments done on aging mice with the protein GDF11. GDF11 is what’s known as a growth factor, a molecule that binds to receptors on stem cells and tells them what kind of differentiated cell they’re supposed to become. It had been determined via a prior screening process that GDF11 levels decline in elderly mice, making it a prime target for anti-aging stem cell research. It didn’t hurt that the protein had already been implicated in a number of different healing and developmental processes.
The Harvard team tried two approaches to boosting levels of GDF11 in old mice. One of these involved surgically combining the circulatory systems of an old mouse and a very young mouse, such that the old mouse was receiving young blood. The second (and less creepy) method involved simple injections of the growth factor. The result of both methods was the same: young hearts in old mice. Specifically, the heart muscle thickening and stiffening known as hypertrophy that’s often seen in aging heart tissue was reversed. If replicated in humans, the effect would be akin to curing diastolic heart failure, a common cause of death in the elderly.
Image: the left reconstruction is of blood vessels in an old mouse's brain, and the right is of an old mouse with new blood/Lida Katsimpardi/Science
Those heart tissue results were completely out of the blue. Richard T. Lee, a cardiologist and co-lead author of the 2013 study, told Nature, “We did this pretty much as a long-shot experiment to see if there was some pathway that would give us insight into the heart-ageing process. We were just totally stunned when it worked.”
The study out today basically just expands on last year’s revelation using two additional markers: exercise capability (skeletal muscles) and improved olfactory functioning (the brain). The functional improvements were significant within both sorts of tissue, but the effect is deeper than tissue regeneration and repair.
"The additional piece is that while prior studies of young blood factors have shown that we achieve restoration of muscle stem cell function and they repair the muscle better, in this study, we also saw repair of DNA damage associated with aging,” explains Amy Wagers, the current study’s lead author, in a press release. “And we got it in association with recovery of function, and we saw improvements in unmanipulated muscle. Based on other studies, we think that the accumulation DNA damage in muscle stem cells might be reflect an inability of the cells to properly differentiate to make mature muscle cells, which is needed for adequate muscle repair.”
With DNA repaired and all of that accumulated genetic junk removed, it may be possible for revitalized tissue to repair itself in the future, as if it were young. "I don't think we fully understand how this happening or why,” says Wagers. “We might say that the damage is modification to the genetic material; the genome does have breaks in it. But whether it's damaging, or a necessary part of repair, we don't know yet."
The researchers are currently in negotiations with a venture capital firm to obtain funding to do the necessary pre-clinical trials before beginning trials using human subjects. It would seem that we’re talking about a matter of years, rather than decades, before GDF11 is at least treating the specific diseases of old age, like Alzheimer’s and diastolic heart failure, if not the soon-to-be disease of old age itself.