 The advancements in healthcare and lifestyle have resulted in increased focus on age-related diseases such as neurodegeneration, cardiovascular disease, frailty, and arteriosclerosis, which involve protein, lipid or nucleic acid modifications including cross-linked and non-degradable aggregates like advanced glycation end products, ages. Formation of endogenous or uptake of dietary ages can lead to further protein modifications and activation of inflammatory signaling pathways. This review provides an overview of the most prominent age-mediated signaling cascades, age-receptor interactions, prevention of AGE formation, and the impact of ages during pathophysiological processes. This article was authored by Christian Ott, Kathleen Jacobs, Alisa Hauke, and others.