Recently, it has been proposed that the receptor for advanced glycation end-products (RAGE) plays a crucial
role in damaging cellular processes, such as neuroinflammation, neurodegeneration, excitotoxicity and oxidative stress.
RAGE is a multiligand receptor belonging to the immunoglobulin superfamily of cell surface molecules acting as a
counter-receptor for diverse molecules. Engagement of RAGE converts a brief pulse of cellular activation into sustained
cellular dysfunction and tissue damage. Indeed, the involvement of RAGE in physiopathological processes has been
demonstrated for several neurodegenerative diseases. It is the full-length form of RAGE the one constituting the cellular
receptor which is able to activate intracellular signals. After the binding of ligands to RAGE, oxidative stress is increased;
then, over-expression of RAGE produces vicious cycles that perpetuate oxidative stress and contribute to
neuroinflammation by nuclear factor-kB (NF-kB) up-regulation. The NF-kB activation promotes the expression of proinflammatory
cytokines, including RAGE expression, to induce a prolonged activation and promotion of signaling
mechanisms for cell damage. Because inflammatory and oxidative events have been demonstrated to concertedly interact
during neurodegenerative events, this review is aimed to discuss the role of RAGE as mediator of an interaction between
inflammation and oxidative stress through NF-kB signaling pathway.