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Current Alzheimer Research

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Review Article

RAGE Isoforms, its Ligands and their Role in Pathophysiology of Alzheimer’s Disease

Author(s): Rani C. Chellappa, Rani Palanisamy* and Karthikeyan Swaminathan

Volume 17, Issue 14, 2020

Page: [1262 - 1279] Pages: 18

DOI: 10.2174/1567205018666210218164246

Price: $65

Abstract

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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