ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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  • Review Article   
  • J Alzheimers Dis Parkinsonism 2018, Vol 8(1): 421
  • DOI: 10.4172/2161-0460.1000421

The Receptor for Advanced Glycation Endproducts (RAGE) and Mediation of Inflammatory Neurodegeneration

Julia Derk, Michael MacLean, Judyta Juranek and Ann Marie Schmidt*
Diabetes Research Program,Division of Endocrinology, Diabetes and Metabolism, NYU School of Medicine, , 550 First Avenue, Smilow 906, New York, USA
*Corresponding Author : Ann Marie Schmidt, Diabetes Research Program, Division of Endocrinology, Diabetes and Metabolism, NYU School of Medicine, 550 First Avenue, Smilow 906, New York, USA, Tel: 212 263 9444, Email: AnnMarie.Schmidt@nyumc.org

Received Date: Jan 06, 2018 / Accepted Date: Jan 17, 2018 / Published Date: Jan 24, 2018

Abstract

The Receptor for Advanced Glycation Endproducts (RAGE) is an immunoglobulin-type, transmembrane receptor that is expressed on numerous cell types in the Central Nervous System (CNS) and periphery, such as neurons, astrocytes, microglia, mononuclear phagocytes, epithelial cells and endothelial cells (ECs). RAGE binds a discrete repertoire of ligands, including non-enzymatically glycated proteins and lipids, also known as advanced glycation endproducts (AGEs), for which the receptor is named, in addition to multiple members of the S100/calgranulin family, oligomeric forms of Aβ, high mobility group box 1 (HMGB1), phosphatidylserine (PS) and lysophosphatidic acid.

Keywords: Alzheimer’s disease (AD); Cerebrovascular ischemia (CI); Parkinson’s disease (PD); Amyotrophic lateral sclerosis (ALS); Dementia

Citation: Derk J, MacLean M, Juranek J, Schmidt AM (2018) The Receptor for Advanced Glycation Endproducts (RAGE) and Mediation of Inflammatory Neurodegeneration. J Alzheimers Dis Parkinsonism 8: 421. Doi: 10.4172/2161-0460.1000421

Copyright: ©2018 Derk J, 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.

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