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Ligands of Receptor for Advanced Glycation End-Products Produced by Activated Microglia are Critical in Neurodegenerative Diseases
Myeongjoo Son1,2* Seyeon Oh2*, Sojung Lee1,2 and Kyunghee Byun1,2†1Department of Anatomy and Cell Biology, Gachon University, Graduate School of Medicine, Incheon, Republic of Korea
2Functional Cellular Networks Laboratory, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Republic of Korea
- Corresponding Author:
- Kyunghee Byun
Department of Anatomy and Cell Biology
Gachon University Graduate School of Medicine
Yeonsu-Gu, Incheon 21999, Republic of Korea
Tel: + 82-899-6511
E-mail: khbyun1@gachon.ac.kr
Received date: March 17, 2017; Accepted date: April 03, 2017; Published date: April 10, 2017
Citation: Son M, Oh S, Lee S, Byun K (2017) Ligands of Receptor for Advanced Glycation End-Products Produced by Activated Microglia are Critical in Neurodegenerative Diseases. J Alzheimers Dis Parkinsonism 7:318. doi:10.4172/2161-0460.1000318
Copyright: © 2017 Son M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Receptor for advanced glycation end products (RAGE) and its ligands have been reported to be involved in the progressions of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease. Recently microglia activated by immunological stimuli, cytokines, or oxidative stress were reported to synthesize and secrete RAGE ligands including AGEs, HMGB1, and S100 in neurodegenerative diseases. Furthermore, RAGE/ligand binding has been implicated in neuroinflammation and in the progression of neurodegenerative diseases through a RAGEmediated pathway in neurons. A number of RAGE inhibitors, such as, antagonists, small RAGE inhibitors, anti-RAGE antibody, and soluble RAGE, have been shown to interfere with RAGE/ligand binding and to reduce RAGE ligand accumulation, microglia activation, and neuronal cell death in neurodegenerative diseases. Accordingly, RAGE inhibitors present an attractive therapeutic target in neurodegenerative diseases, and RAGE ligands might be useful diagnostic targets. Some human studies have shown RAGE ligand distributions in brain, serum, and cerebrospinal fluid are promising biomarkers for early disease detection and that these ligands might play important roles during early disease stages. Taken together, RAGE ligands and RAGE inhibitors appear to be good therapeutic and diagnostic candidates for neurodegenerative diseases.
