RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer's disease | Zendy

ShiDu Yan Shirley | Zendy

AI Assistant Blog Pricing

Home ZAIA Blog

Open Access

RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer's disease

Author(s) -

ShiDu Yan Shirley

Publication year - 2011

Publication title -

frontiers in bioscience-scholar

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.606

H-Index - 46

eISSN - 1944-7906

pISSN - 1945-0516

DOI - 10.2741/265

Subject(s) - rage (emotion) , neuroscience , microglia , pathogenesis , receptor , glycation , alzheimer's disease , medicine , microbiology and biotechnology , biology , disease , immunology , inflammation

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 beta-peptide (Abeta)-mediated cellular perturbation relevant to the pathogenesis of Alzheimer's disease (AD). The interaction of RAGE with Abeta in neurons, microglia, and vascular cells accelerates and amplifies deleterious effects on neuronal and synaptic function. RAGE-dependent signaling contributes to Abeta-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 Abeta-induced cellular perturbation.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research