AI Used to Generate Immune System “Clock” that Predicts Health and Mortality

Investigators at Stanford University School of Medicine and the Buck Institute for Research on Aging have harnessed artificial intelligence to build an inflammatory-aging clock—iAge— that they suggest is more accurate than the number of candles on your birthday cake in predicting how strong your immune system is, how soon you’ll become frail, or whether you have—as yet unseen—cardiovascular problems that could in the future become clinically relevant.

Through their work with the 1000 Immunomes Project, and other cohorts, the scientists also identified a chemokine associated with cardiac aging, which they suggest could be used for the early detection of age-related pathology, and could also represent a potentially modifiable target for intervention.

“Standard immune metrics which can be used to identify individuals most at risk for developing single or even multiple chronic diseases of aging have been sorely lacking,” said David Furman, PhD, Buck Institute associate professor and director of the Artificial Intelligence Platform, director of the 1001 Immunomes Project at Stanford University School of Medicine, a visiting scholar at Stanford’s Institute for Immunity, Transplantation and Infection, and senior author of the team’s study, which is published in Nature Aging. “Bringing biology to our completely unbiased approach allowed us to identify a number of metrics, including a small immune protein which is involved in age-related systemic chronic inflammation and cardiac aging. We now have means of detecting dysfunction and a pathway to intervention before full-blown pathology occurs.”

The team published its findings in a paper titled, “An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging.” Lead authors of the study are Nazish Sayed, MD, PhD, assistant professor of vascular surgery at Stanford, and Yingxiang Huang, PhD, senior data scientist at the Buck Institute.

“Every year, the calendar tells us we’re a year older,” Furman explained. “But not all humans age biologically at the same rate. You see this in the clinic—some older people are extremely disease-prone, while others are the picture of health.” This divergence, Furman said, traces in large part to differing rates at which people’s immune systems decline. The immune system, which has evolved to deal with threats such as injuries or infection by pathogens, excels at mounting a quick, intense, localized, short-term, resist-and-repair response called acute inflammation. This positive inflammatory response typically does its job, then wanes within days. But, as the authors noted, while the important role of the immune system in the maintenance of human health and protection against infections has been recognized for over a hundred years, “ … it was only in the past few decades that it has become apparent that inflammatory components of the immune system are often chronically elevated in aged individuals and associated with an increased incidence of cancer, cardiovascular disease, neurodegenerative disorders, and others.” And these observations have led to the concept that inflammation plays a critical role in regulating physiological aging.

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