Rage isoforms, its ligands and their role in pathophysiology of alzheimer’s disease

Rani C. Chellappa, Rani Palanisamy, Karthikeyan Swaminathan

Research output: Contribution to journalReview articlepeer-review

9 Scopus citations

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 RAGE-Aβ interaction and the role of RAGE as a potential target in the development of treatments for AD.

Original languageEnglish (US)
Pages (from-to)1262-1279
Number of pages18
JournalCurrent Alzheimer Research
Volume17
Issue number14
DOIs
StatePublished - 2020
Externally publishedYes

Keywords

  • Alzheimer’s disease
  • Amyloid beta
  • Inflammation
  • Ligands
  • RAGE isoforms
  • Reactive oxygen species
  • Receptor for advanced glycation end product
  • Therapeutic target

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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