Receptor for Advanced Glycation End product (RAGE) plays a crucial role in a variety of
physiological and pathological processes due to its ability to bind a broad repertory of ligands. There
are also multiple forms of RAGE that exist; some work on promoting feed-forward pathways while
others perform inhibitory actions. This review focuses on the RAGE isoforms expression, its
intracellular pathways activation via RAGE- ligand interaction, and its importance in the physiological
and pathological process of the brain. Many studies have suggested that RAGE induces the
pathophysiological changes in Alzheimer’s disease (AD) by being an intermediator of inflammation
and inducer of oxidative stress. The critical roles played by RAGE in AD include its involvement in
amyloid-beta (Aβ) production, clearance, synaptic impairment, and neuronal circuit dysfunction.
RAGE-Aβ interaction also mediates the bi-directional crosstalk between peripheral and central
systems. This interaction underlies a potential molecular pathway that disrupts the material structure
and physiology of the brain. This review highlights the structure-function relation for RAGEAβ
interaction and the role of RAGE as a potential target in the development of treatments for AD.
Keywords: Receptor for advanced glycation end product, RAGE isoforms, ligands, amyloid beta, inflammation, Alzheimer's
disease, reactive oxygen species, therapeutic target.
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