 The increased focus on age-associated diseases such as neurodegeneration, cardiovascular disease, frailty, and arteriosclerosis has led to improvements in health care and lifestyle resulting in elevated lifespan. Protein, lipid, or nucleic acid modifications are involved in these chronic diseases, including cross-linked and non-negratable aggregates such as advanced glycation end products, ages. Formation of endogenous or uptake of dietary ages can lead to further protein modifications and activation of several 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 Kristi Annott, Kathleen Jacobs, Alisa Hauke, and others.