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Mol Neurobiol. 2018 Feb;55(2):1463-1476. doi: 10.1007/s12035-017-0419-4. Epub 2017 Feb 6.

RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration.

Author information

1
Department of Basic Medical Sciences, Wrocław Medical University, Wrocław, Poland.
2
Facultad de Ciencias de la Salud, Universidad San Sebastián, Lientur, Concepción, Chile.
3
Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá D.C., Colombia.
4
Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile.
5
Clinic of Psychiatry, Wrocław Medical University, Pasteura 10, 50-367, Wrocław, Poland. jerzy.leszek@umed.wroc.pl.

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.

KEYWORDS:

Chronic inflammation; Neurodegeneration; Rage; Self-perpetuated stimulation; TLR

PMID:
28168427
DOI:
10.1007/s12035-017-0419-4
[Indexed for MEDLINE]

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