New research from the Stanford University School of Medicine and the Buck Institute for Research on Aging is demonstrating a new tool that can calculate a person’s immune system age. The findings suggest tracking the degree of low-grade chronic inflammation that appears as we age could help predict frailty and disease before symptoms appear.
“Every year, the calendar tells us we’re a year older,” explains David Furman, senior author on the new study published in Nature Aging. “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.”
As we age our immune system can become dysfunctional. Not only is it less effective at mounting a strong response against pathogens but it also begins to mistakenly target normal cells.
One hypothesis argues that the chronic, low-grade systemic inflammation generated by an aging immune system plays a major role in the development of many age-related diseases. But until now there hasn’t been any way to measure this low-grade inflammation and predict who is immunologically aging faster and more at risk of age-related disease.
Beginning over a decade ago the research recruited 1,001 subjects aged between nine and 96. Called the 1000 Immunomes Project, the ongoing study is designed to track the relationship between immune system decline and aging.
Using an AI algorithm a pattern of blood-based inflammatory biomarkers was developed to quantify a person’s immune system age. The resulting measure has been dubbed iAge. Age-related systemic inflammation has been linked with an older iAge score, and iAge was effectively associated with the risk of developing cardiovascular disease.
“Our inflammatory aging clock’s ability to detect subclinical accelerated cardiovascular aging hints at its potential clinical impact,” says Furman. “All disorders are treated best when they’re treated early.”
Interestingly, the researchers also homed in on one specific inflammatory biomarker that seemed to influence a person’s iAge more than any other single molecule. Called CXCL9, this immune molecule works to attract other immune cells to a specific location in the body.
The researchers discovered CXCL9 levels rise significantly from the age of 60, and high CXCL9 levels were associated with signs of cardiovascular disease. Subsequent animal tests found inhibiting CXCL9 activity reversed age-related abnormalities in key blood vessel cells.
The implications of this new research are broad. An objective blood-based test measuring a patient’s immune system age could be a useful clinical tool for tracking those at high risk of developing age-related disease. This could allow doctors to implement preventive health measures at early stages. The discovery of an association between CXCL9 levels and age-related disease also helps direct researchers toward new treatments for a number of conditions.
“… we have identified a metric for systemic chronic age-related sterile inflammation which tracks with multiple disease phenotypes in multiple cohorts and thus, could be used as a metric for healthy versus unhealthy aging,” the researchers write in the study. “Our results also demonstrate a link between inflammatory molecules of the immune system and vascular biology.”
The new study was published in the journal Nature Aging.
Source: Stanford University
