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What is it?

iAge is a technology developed to detect inflammatory patterns in the body to predict the risk of someone developing a disease. According to LiveScience, this is mainly done through the use of artificial intelligence (A.I). By detecting chronic inflammation in one's body, researchers can find someone's "immunological age" and determine when someone will become frail.

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How does it work?

According to a recent study published Monday July 12th, 2021, in the journal Nature Aging, a deep neural network can evaluate blood-borne signs of inflammation. According to Medical News Today, Cytokines are proteins that carry communications between immune cells and other cells in the body. This study done by Sayed, N., Huang, Y., Nguyen, K. et al. found a link between the inflammatory clock of aging (iAge) and total disease, lifespan, and immunological degradation by analyzing blood samples from 1,001 people aged 8 to 96 years. This data was then used to create reference values. In comparison to a set of reference values and in proportion to their age in years, an iAge score provides individuals with their age based on immunological health and inflammatory levels. An increased risk of disease is indicated by a higher iAge score, whereas a lower score implies a generally robust immune system. A cytokine named CXCL9 had the most significant impact on a person's iAge score after analyzing 50 cytokines. CXCL9 is typically used to attract immune cells to the location of an infection, but levels of the molecule began to rise dramatically in the research participants around the age of 60. The team connected this age-related cytokine surge in lab dishes in endothelial cells found in blood vessel walls.

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CXCL9, being a solid contributor to aging endothelial cells, created poor vascular function and cardiac aging. David Furman, chief of the Center for AI and Data Science of Aging at the Buck Institute for Research on Aging, stated that from the research done in lab dishes, When the genes for CXCL9 are taken out, the cells' functions are restored, allowing them to contract and form vascular networks as they should. This suggests that the cytokine is, in fact, a solid contributor to iAge. According to the authors of the study, this indicates that future medical treatments could be created to prevent age-related increases in CXCL9.

Article Authors: Idil Gure, Maria Giroux

Article Editor: Valerie Shriobokov