RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration

Overview

Journal Mol Neurobiol

Specialties Molecular Biology
Neurology

Date 2017 Feb 8

PMID 28168427

Citations 49

Authors

Kazimierz Gasiorowski

Barbara Brokos

Valentina Echeverria

George E Barreto

Jerzy Leszek

Affiliations

Soon will be listed here.

Abstract

Chronic inflammatory reactions are consistenly present in neurodegeneration of Alzheimer type and are considered important factors that accelerate progression of the disease. Receptors of innate immunity participate in triggering and driving inflammatory reactions. For example, Toll-like receptors (TLRs) and receptor for advanced glycation end product (RAGE), major receptors of innate immunity, play a central role in perpetuation of inflammation. RAGE activation should be perceived as a primary mechanism which determines self-perpetuated chronic inflammation, and RAGE cooperation with TLRs amplifies inflammatory signaling. In this review, we highlight and discuss that RAGE-TLR crosstalk emerges as an important driving force of chronic inflammation in Alzheimer's disease.

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