Most of us think we know what aging looks and feels like. It blurs vision, makes joints creaky, causes things to wrinkle and sag.
But scientists are cataloging far subtler signs of biological aging. It’s a story told not just in the body’s organs but in its genes, cells and proteins — even in the bacteria that colonize us.
First, one or two molecular processes fall out of whack. Those failures send broader functions off kilter. Sometimes all at once, sometimes gradually, our organs suffer and entire networks — the immune system, for instance — begin to falter.
Understanding how all this happens could allow us to live longer someday. But defining what aging is and exactly how it progresses may enable us to stay healthy for more of our lives.
Two new pieces of research bring that goal of extending humans’ “healthspan” a bit closer. Both identify biomarkers that help define what it means, at a microscopic level, to age. Both zero in on mechanisms prone to break down as we age — in other words, targets for therapies that could disrupt or delay the aging process.
In one of the new studies, Stanford University researchers combed through 18 million data points collected from 106 people. Emerging from that study, published in the journal Nature Medicine, is the idea that individuals age along at least four distinct biological pathways. While one person may be most prone to decline in the function of his kidneys, another may experience the most age-related degradation in the liver, the immune system or in metabolic function, the findings suggest.
Most of us likely age along some or all those fronts, if not more, said Stanford geneticist Michael Snyder, who led the research. But classifying people by their personal “aging style,” or areas of greatest vulnerability, may help them identify and forestall their most likely depredations of aging, he said.
In the second study, scientists from the Buck Institute for Research on Aging profiled the known universe of tissues and cells that can reveal the biological age of the human body. It made use of data collected as part of a study that has tracked 3,200 volunteers since 1958. That atlas of aging’s biomarkers will speed efforts to find and develop drugs that could slow biological aging, said University of Southern California biochemist Judith Campisi, who led the work published in PLOS Biology. One day, she added, it may allow doctors to give their patients “a clear readout of how well, or poorly, their various tissues and organs are aging.”
Scientists have honed in on “senescent” cells, which stop dividing under stress, as a key driver of conditions such as cancer, heart disease, diabetes, arthritis and dementia. Since these diseases are more common as we get older, they and their root causes have become central to scientists’ understanding of aging. Researchers suspect that when you disrupt the development of one disease of aging, you may help protect against others.
“I can envision a world in which everyone gets their ageotype measured, so that at the earliest sign of acceleration, you can intervene,” Snyder said.