Abstract

A broad spectrum of diseases that become more prevalent with aging – ranging from diabetes and neurodegenerative disorders to atherosclerosis, arthritis, increased cancer incidence, and heightened susceptibility to infections – can often be traced back to or exacerbated by two interconnected phenomena: inflammaging and immunosenescence. Inflammaging refers to the chronic, low-grade inflammation that typically accompanies aging, while immunosenescence involves the gradual deterioration of the immune system’s function over time.

This project is designed to mechanistically unravel the intricate relationship between inflammaging and immunosenescence throughout the aging process. We will employ a combination of state-of-the-art techniques, including single cell multi-omics, alongside transgenic mouse models and organoid culture systems. These tools will help us investigate how the gradual decline in homeostatic functions of critical cell populations – such as those involved in maintaining tissue integrity and immune response – affects the progression of immunosenescence and systemic inflammation in the body.

Our primary research questions are twofold: First, we seek to determine the extent to which deteriorating homeostatic functions influence the onset and progression of immunosenescence and inflammation in peripheral tissues. Second, we aim to identify the systemic interactions between these cellular changes and their impact on overall inflammatory and immune responses during natural aging.

By adopting a systems biology perspective, our study aims to integrate these findings into a comprehensive model of aging. This approach will help us uncover novel therapeutic targets and intervention strategies that could mitigate the adverse effects of aging, thereby enhancing overall health and promoting healthier aging outcomes.