Frontiers in Bioscience-Scholar (FBS) is published by IMR Press from Volume 13 Issue 1 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
, Doris Chen 1, Shiqian Yan 1, Lan Guo 1, John Xi Chen 51 Department of Surgery, Physicians and Surgeons College of Columbia University, New York, NY 10032
2 Department of Pathology and Cellular biology, Physicians and Surgeons College of Columbia University, New York, NY 10032
3 Taub Institute for Research on Alzheimer Disease and the Aging Brain, Physicians and Surgeons College of Columbia University, New York, NY 10032
4 Department of Pharmacology and Toxicology and Higuchi Bioscience Center, University of Kansas, Lawrence, KS 66047-3729
5 Department of Neurology, Memorial Sloan-Kettering Cancer Center, New York, NY10065
*Author to whom correspondence should be addressed.
Abstract
RAGE, a receptor for advanced glycation endproducts, is an immunoglobulin-like cell surface receptor that is often described as a pattern recognition receptor due to the structural heterogeneity of its ligand. RAGE is an important cellular cofactor for amyloid β-peptide (Aβ)- mediated cellular perturbation relevant to the pathogenesis of Alzheimer’s disease (AD). The interaction of RAGE with Aβ in neurons, microglia, and vascular cells accelerates and amplifies deleterious effects on neuronal and synaptic function. RAGE-dependent signaling contributes to Aβ-mediated amyloid pathology and cognitive dysfunction observed in the AD mouse model. Blockade of RAGE significantly attenuates neuronal and synaptic injury. In this review, we summarize the role of RAGE in the pathogenesis of AD, specifically in Aβinduced cellular perturbation.
Keywords
- Amyloid beta
- RAGE
- Alzheimer Disease
- Inflammation
- Review